And if you need combination therapy, you'd preferably add a DHP CCCB over adding a thazide diuretic. A loop diuretic would come in specifically if the patient has CKD with volume overload.

Okay. And if a diabetes is without those specific complications,

then the initial choices are broader. ACI, ARBs, DHP, CCBs, or thioid thioid like diuretics are all considered acceptable for line option

more choice there.

Yeah. But for combination therapy in this group, an ACI plus DHP CCB combination is still preferred over an ACI plus thioide combo.

Interesting preference even without complications. Gota.

Okay. Moving to cardiovascular disease itself. Patients with CAD

for coronary artery disease. ACIs or ARBs are the drugs of choice. Beta blockers or CCBs can be added if needed to manage stable angina symptoms.

For combination therapy in high-risisk CAD patients that ACID HP CCB combination is again preferred. There's a caution mentioned about being careful not to lower SBP too much if the DBP is already quite low. Say 60 millm HG especially in patients with LVH could potentially compromise coronary profusion.

Good point. What about after a recent heart attack and MI

standard of care there is beta blockers plus ACIs or ARBs if the patient is ACI intolerant. A long acting CCB can be used if beta blockers are contraindicated or ineffective.

Okay.

But importantly avoid non DHP CCBs like verapamil or diliasm if the patient also has concominant heart failure

right crucial interaction there so speaking of heart failure

the foundation of therapy for HFREF heart failure with reduced ejection fraction is ACIS or ARBs if intolerant plus beta blockers

the core combo

absolutely then aldoststerone antagonist like spironolactone or epernon can be added in selected patients maybe those with recent HF hospitalization recent MI elevated BNP or NTROBBN or symptomatic HF and YHA class 24thbazide or loop diuretics are used as additive therapy but specifically for managing volume overload not as core mortality drugs.

Got it. And there's that newer combination.

Yes. The AR9 the combined ARB neprolysin inhibitor Volso tensacubetrol. It's recommended in symptomatic HFREF patients who are already on standard therapy actually replacing the ACI or ARB.

Okay. Replacing the ACIB.

Yeah. You need to titrate these doses up to the levels proven effective in clinical trials and be really vig ent about monitoring potassium and renal function when you're combining ACI or baldsterone antagonist

potassium risk

definitely the ACI plus ARB combo is technically possible as a secondline strategy in select HF patients but it requires super careful monitoring because of that hypercalemia risk and if ACRBs are contraindicated or not tolerated at all the combination of hydrolysine and isolate denotrate is an option

you got lots of options at heart failure what about left ventricular hypertrophy LVH

for LVH the preferred classes are are ACI, ARB, long-acting CCB or thioid like diuretics. The guidelines specifically say to avoid hydrolysine minoxidil in these patients.

The avoid hydrolysine and minoxidil with LDH.

Got it.

After a stroke or TIA,

the specifically recommended combination therapy is an ACI plus a thazy or thazidelike diuretic.

That specific congo.

Yes. The guidelines also advise avoiding routine BP treatment in the acute phase of a stroke unless the BP is extremely high like over120. And once again avoid that ACI plus ARB combination.

Okay. Non-diabetic chronic kidney disease CKD with proteinuria.

AC inhibitors are first line there or ARBs if ACI intolerant. Diurax are added as needed. And again close monitoring of renal function and potassium is essential with ACB use. And say it with me.

Avoid the ACI plus ARB combo.

Exactly.

What about peripheral arterial disease? P AD.

PA itself doesn't really change the initial anti-hypertensive treatment choices, but the guidelines do caution against using beta blockers in patients with severe P AD.

Okay. And renovvascular disease like renal artery stenosis.

You can use ACIs or ARBs, but you have to exercise significant caution, especially if you suspect bilateral renal artery stenosis because there's a real risk of causing acute renal failure. Need specialist input often,

right? Caution needed there. Yeah.

And we absolutely have to mention pregnancy and potential pregnancy.

Oh, critically important. ACIs and ARBs are parodogenic absolutely contraindicated in pregnancy.

Preconception counseling is strongly recommended for women on these medications who could become pregnant. During pregnancy, the recommended drugs generally include letool, methyl-dopa, and long acting oral nitipene. Some other beta blockers might be used too

and second line in pregnancy.

Hydrolysine, clonodine, and thiocyes are considered second line options during pregnancy.

What about breastfeeding?

For women who are breastfeeding, options generally considered compatible include leettool, methylopa, long acting oral nifetapene and even the acceis and elapal or captipril.

Good to have those lists.

Yeah.

Okay. That's a really comprehensive look at drug choices based on compelling indications. But as pharmacists, we know managing therapy isn't just picking the right drug.

Definitely not.

It's also about anticipating and managing potential issues, side effects. The ARCs vigilance info in this source highlights some key points here.

Yeah, really practical stuff for ACIS and ARBs. As we just hammered home, the absolute Biggest warning is terodogenicity contraindicated in pregnancy. Caution in women of childbearing potential. Right.

ACIs are of course notorious for causing that dry cough. Both classes can cause hypercalemia. And although it's rare, the serious side effect of angiodma,

okay, beta blockers.

Remember, not firstline monotherapy for patients age 60 and up. Common side effects can include sexual dysfunction, particularly in males, CNS effects like depression, nightmares, or insomnia. And they can potentially cause hypoglycemia or worsen glucose control especially in patients with diabetes.

Good points. Long acting CCBs.

A specific caution here is to generally avoid routinely combining a non-dp CCB like verapram or diliasm with a beta blocker because it increases the risk of brady cardia and heart block

right that interaction.

And always avoid short acting nephipine. Common side effects people complain about are flushing, headache and that characteristic lower limb edema.

Yes, the swollen ankles.

Yeah,

thazy diuretics.

Preference for the longer acting ones like indapamide and chloraladone.

And you'd want to temporarily withdraw them if a patient gets dehydrated like with vomiting or diarrhea.

Okay.

Common side effects include sexual dysfunction in both males and females, electrolyte issues like hypocalemia, low potassium, hyponetriia, low sodium, hypomagnesmia, low magnesium, and also hyperasemia which can potentially trigger gout attacks in susceptible people.

Lots to monitor there. Okay, so Let's say you've followed the algorithms, considered the compelling indications, started therapy, maybe added a second or third drug, but the patient's BP is still above target. What's next?

Right now, you need to start thinking about resistant hypertension.

And how is that defined?

It's specifically defined as blood pressure remaining above the target despite the patient taking three or more anti-hypertensive medications at optimal doses.

Okay, three or more drugs.

And crucially, that regimen should preferably include a diuretic. Usually, that means a R s blocker like an ACI or ARB, a CCB and a diuretic are already on board.

But before you jump to labeling it as truly resistant,

yes, absolutely. Essential first step, rule out pseudo resistance. This is super common and a critical thing to check.

Pseudo resistance, meaning it looks resistant but isn't really.

Exactly. It means the high readings might be due to something else entirely. You have to check for inaccurate measurement. Go right back to basics. Check their technique, their machine. Check for non-adherence.

Are they actually taking the medications as prescribed or sticking to the lifestyle changes, right?

Could there be unidentified secondary hypertension? Is the drug regimen itself suboptimal? Maybe wrong combinations or doses. Are there significant drug interactions happening?

Ah, drug interactions. What are some common culprits that can raise BP?

The source lists quite a few. NSADs are a big one. Oral contraceptives, corticosteroids, elicit substances like cocaine or amphetamines. Orthropoin used for anemia. suppressants like cyclesporine or tacarolamus. Even things like excessive licorice consumption.

Licorice.

Yeah. Also, watch out for certain over-the-counter supplements, oral decongestants like pseudoine that are at cold meds and some anti-depressants, particularly MAIs or sometimes SSRIs depending on the specific drug and patient.

Okay, lots to screen for there. What else causes pseudo resistance?

Well, also rule out associated conditions that contribute things like obesity, obstructive sleep apnea, chronic pain, or maybe unmanaged mental health issues like anxiety and don't forget simple volume overload from eating too much salt.

So, you rule all that out.

If you've thoroughly ruled out all those factors and the BP is genuinely resistant despite optimal therapy with three or more drugs, including a diuretic, then you consider referral to a hypertension specialist.

Okay. And speaking of non-adherence, which you mentioned is a cause of pseudo resistance, the guidelines really emphasize that helping patients actually stick to their therapy requires well a multi-pronged approach.

It really does. Simplifying the medication regimen is huge, which again highlights the value of those SPCs, single pill combinations whenever possible,

themselves to take.

Exactly. Tailoring how and when they take their pills to fit their daily routine, involving the patient setting their own BP goals, maybe empowering them with self-monitoring. These are all key strategies.

And it's vital, isn't it, to actually review adherence to both the meds and the lifestyle stuff before you start changing the therapy regimen. absolutely critical. Don't just add another drug if they're not taking the ones they already have. Other things that can help include out of office contact like phone calls or messages, coordinating care with other providers like community pharmacists, and using electronic aids like reminder apps or smart pill bottles.

Makes sense. Finally, let's quickly touch on follow-up. Once someone's diagnosed and on treatment, how often should you be checking in?

Okay, for follow-up measurements, you generally use standardized office BP, preferably with electronic devices. If white code effect was confirmed earlier, ABPM or HBPM can actually be used for follow-up monitoring, too.

And the frequency,

it really depends on whether the BP is at target or not. If the patient's BP is not yet at target, you should probably see them relatively frequently, say every 1 to two months, and you continue that until they reach their target on two consecutive visits.

Okay, frequent follow-up until controlled. And once BP is consistently at target,

then the follow-up intervals can usually be extended maybe to every 3 to 6 months. Follow-up specifically for reinforcing the health behavior modifications should also happen regularly, maybe every 3 to 6 months as well.

But you always need to adjust based on the individual, right?

Oh, absolutely. Adjust the follow-up frequency based on the whole clinical picture. Patients who are symptomatic, have very severe hypertension, maybe experience drug intolerance issues, or have significant target organ damage will likely need much shorter follow-up intervals.

Okay, great. Wow, that was quite a deep dive. We covered uh accurate measurement techniques and those crucial thresholds, evaluating the patient beyond just the numbers, understanding treatment targets based on risk levels.

Mhm.

The critical role of health behaviors, navigating those pharmacological algorithms and tailoring therapy based on compelling indications,

right? Key drug class considerations, how to approach resistant hypertension, strategies for improving adherence, and managing followup.

Yeah. Hopefully knowing these specific details directly from the guidelines and supporting materials provides some real clarity. It can, you know, give you peace of mind knowing you're equipped with the crucial information for the PBC and for practice.

Absolutely. And remember, this deep dive was brought to you by Pharma Board Group based on that essential CTC reference.

Okay. Now, let's test your recall on one key detail we covered today pulled straight from the source material. Based on the Hypertension Canada guidelines, which blood pressure measurement method is the preferred out of office method for the diagnosis of hypertension?

Okay. Is it A. OBPM, office blood pressure measurement. B, AOBP, automated office blood pressure.

C, ABPM, ambulatory blood pressure monitoring. D, HBPM, home blood pressure monitoring.

Think about that for a moment. Preferred out of office for diagnosis.

And finally, just to leave you with something to think about, considering just how much individualization is needed when managing hypertension, you know, based on a patient's unique characteristics, their other medical conditions, what specific patient factor or coorbidity that we discussed today do you think presents the most complex challenge when you're trying to choose their anti-hypertensive therapy? Something to mull over as you continue your studies.

ترانسکریپت مبحث آنژین پایدار
Welcome to the deep dive, your go-to for cutting through the noise and getting straight to what matters. If you're a Canadian pharmacist PEBC candidate, uh this deep dive, it's customtailored just for you. Today, we're really going to unravel the complexities of stable anggina. We're pulling key insights, you know, directly from the therapeutic choices chapter. We'll distill those essential medication algorithms, the vital tables, and yeah, the practical tips you'll absolutely need both for exam success and for realworld clinical practice. Our mission here is simple. Give you clarity, accuracy, and some truly actionable insights. Oh, and just so you know, this deep dive is brought to you by the Firmmaboard Group, and it's based on the CTC reference. Okay, let's unpack this.

Exactly. And um our goal isn't just to cover the material, right? It's really about giving you that peace of mind. We're summarizing the absolute critical information, making sure you won't miss, you know, a single crucial detail for your understanding and well, for those allimp important exams.

Perfect. So, let's kick things off right at the beginning for someone needing that rock solid definition for their PBC exam.

What exactly is stable angginaptoris? Can you paint a clear picture for us?

Certainly. So angginapctorus fundamentally it's a squeezing kind of discomfort usually in the chest and it signals myioardial eskemia basically the heart muscle isn't getting enough blood and oxygen for what it needs right then and you know overwhelmingly the root cause is coronary artery disease CAD where plaque narrows the heart's arteries.

Okay. Eskeemia CAD. Got it. Now, what makes it stable is its predictability. This chest discomfort, it reliably pops up with physical exertion or maybe emotional stress. And just as reliably, it fades away with rest or a dose of nitroglycerin. That's the classic calling card, you could say, of stable CAD,

right? That predictability is key. But the heart can be tricky, can't it? Beyond that typical stable angina chest pain, what are some other ways stable CAD might show up? Maybe less obvious ways.

That's a really great point because yeah, CAD isn't always textbook. Besides classic stable angina, it can present as heart failure or um left ventricular systolic dysfunction that's caused by obstructive CAD. It also includes cases where CAD has stabilized after say an acute coronary syndrome or revascularization procedure. And then there's microvascular anggina and even clinically silent CAD that you might just stumble upon. We tend to group these now under the term chronic coronary syndrome.

Chronic coronary syndrome.

And here's something really crucial clinically. While CAD is the usual suspect, you always have to consider other conditions. that can mimic or worsen eskeeia. Think things like tacocardia, really uncontrolled hypertension, severe aortic stenosis, hypertrophic cardiomyopathy, even anemia. Why does this matter so much? Well, imagine treating something like hypertrophic cardiomyopathy with say long acting nitrates that could actually be harmful. So identifying these other factors ensures you prescribe the right treatment and just as importantly avoid the wrong one.

That distinction really highlights the depth of assessment needed, doesn't it? Yeah.

Okay. So with that foundational understanding. What are our main goals when we start thinking about treating stable angina? What are we actually aiming for?

Right? So, when we talk therapy for stable angina, we're looking at three main objectives. First, and this is vital for the patients day-to-day life, improve their quality of life. That means actively decreasing or preventing those angina episodes and boosting their exercise tolerance make them feel better, function better. Second, we aim to minimize the big risks, specifically reducing the risk of cardiovascular death and non heart attacks, MIS. And finally, we absolutely must tackle the modifiable risk factors.

You know, the things that fuel CAD development and progression in the first place.

Makes perfect sense. Improve quality of life, reduce major events, manage risk factors. Got it. So, to achieve those goals, we first need a really thorough diagnostic picture. What are the essential investigations? The tools that help us piece this puzzle together.

Okay. The initial tool, and honestly, probably the most important one, a detailed patient history. You really need to focus on age. sex and the precise characteristics of their chest discomfort. What does it feel like? Where is it? What brings it on? What makes it better? This is paramount for estimating the likelihood of obstructive CAD. And at the same time, you'll pinpoint those modifiable risk factors. Diabetes, dysipidemia, hypertension, smoking, diet, stress, the whole picture.

And you mentioned table one earlier. How does that fit in? Uh

yes, table one in therapeutic choices is incredibly useful here. It helps estimate that CAD likelihood based on age, sex, and symptom type. It even simplifies classifying the pain with three key questions. Is the discomfort subternal? You know, under the birthbone, is it triggered by exertion? Does it get relieved by rest within about 10 minutes? If it's yes to all three, that point strongly to typical angina. Two out of three. Atypical, one or none. Probably non-angginal chest pain. It's a neat framework.

Okay, that's helpful. History first, then table one helps classify. What else?

Beyond the history, a physical exam. You're looking for signs like tacocardia, high blood blood pressure, maybe evidence of atheroscllerotic disease elsewhere like brutes in the neck. Then some routine lab tests, CBC, creatinine, electrolytes, glucose, lipid profile, and hemoglobin A1C. These give you that broader picture of overall health and risk.

Right. The baseline labs.

Exactly. And finally, non-invasive cardiovascular testing. A resting ECG is standard. Of course, an echo cardiogram might be needed if you suspect heart failure or valve issues, but the core here is often physiologic testing. for eskeeia what we usually call stress testing. This involves either exercise on a treadmill or pharmacologic agents like adenosine or dobbutamine combined with ECG echo or nuclear imaging to see how the heart responds. An alternative that's gaining ground is coronary CT angography. It's got great diagnostic and prognostic value especially good for ruling out significant disease.

That's a really comprehensive approach to diagnosis. So once we have that clear picture, what about treatment? You mentioned non-drug approaches first. What are those initial non-farmacologic strategies.

Yeah. The foundation often starts with aggressive lifestyle changes. Seriously aggressive. We counsel patients on regular aerobic exercise, a heart-healthy diet, lots of veggies, fruits, nuts, whole grains, fish, avoiding trans fats is key, and absolutely smoking sessation, plus moderate alcohol, managing stress. For high-risisk patients, especially those maybe with heart failure, too, a structured cardiac rehabilitation program is strongly recommended. Lifestyle is foundational definitely. What about procedures?

Right. Beyond lifestyle, revascularization is the other big non-farmacologic option. That means either perccutaneous coronary intervention, PCI, or angoplasty as many know it or coronary artery bypass graph surgery, CABG. Now, these aren't for everyone. They're indicated mainly to dramatically improve quality of life when meds just aren't cutting it symptom-wise or critically to improve long-term prognosis in folks with high-risisk anatomy like severe left main stenosis or significant block age in all three major arteries, especially if their heart pump function, the LVEF is low.

Okay. So, PCI or CABG for specific situations. Any others?

Well, for those rare patients who really don't respond to meds and aren't candidates for PCI or CIBG, there are some uh investigational non-farmacologic treatments being explored, things like EECP, but they're not standard practice yet.

Okay. So, lifestyle and sometimes procedures lay the groundwork, but often the real day-to-day management, the game changers for stable angana come in pill form. Mhm.

Here's where it gets really interesting. How do we navigate the pharmacologic landscape, especially thinking about drugs to prevent or decrease anggina itself?

It's true. We don't have tons of direct head-to-head trials comparing the main anti-semic drugs, you know, nitrates, beta blockers, calcium channel blockers, CCBs. So, the choice really boils down to the individual patient, their specific situation, the mechanism driving their eskeeia. And this is where your resources like figure one from therapeutic choices, that algorithm, and your detailed drug reference table two become absolutely indispensable. They're your guides. Many specialists cardiologists will typically start with either a beta blocker or maybe a non dihydroparodine CCB as first line and often they'll pair that with a short acting nitrate for those acute attacks or even to use preventively before activity. If that's not enough, well, maybe add a long acting nitrate or if you started with a beta blocker, perhaps add a dihydropodine CCP.

And you mentioned a crucial warning earlier.

Yes, a critical point. If you suspect or confirm vaso spastic anga caused by artery spasm not just fixed blockage you must avoid beta blockers in those specific cases calcium channel blockers and nitrates are the way to go big difference

good reminder okay could you briefly walk us through the main classes then nitrates first

sure nitrates are primarily venodilators they relax the veins by reducing cardiac preload the amount of blood returning to the heart they significantly decrease the heart's oxygen demand less work for the heart they work well for both acute symptom relief and prevention but here's a key concept long acting nitrates. They need a daily 10 12-hour nitrate-free period to prevent tolerance. Usually, that's overnight. For acute pain, sublingual nitroglycerin spray is often preferred over tablets. It might work faster, maybe cause fewer headaches. And always, always advise patients to sit down when taking it. Reduces the risk of feeling lightaded or even fainting. Oh, and headaches. Very common side effect. Expect it even not usually an allergy,

right? Sit down, expect headaches. Got it. Beta blockers.

Beta block. ers. These guys work by reducing heart rate, the force of contraction and blood pressure. All of which lower the heart's oxygen demand. Both types of non- selective like propranolol and beta 1 selective like metaprolol or bisoperal are effective for angina. And crucially, especially for PBC candidates to remember, they also reduce mortality in patients who have reduced left ventricular systolic function like after a heart attack. A vital safety point, never withdraw beta blocker therapy abruptly, especially after long-term or high dose use. You risk rebound tech. cardio worsening angina it can be dangerous you need to taper the dose slowly usually over 10 to 14 days

okay slow taper is key what about calcium channel blockers you mentioned two types

yes CCBs two main flavors first the non-dihydropyodines like verapamil and diliasm they act more centrally kind of like beta blockers reducing heart rate and contractility good firstline anti-angginals but big caution avoid them in patients with significant left ventricular systolic dysfunction and use care Hopefully if there's underlying AV nodal disease then you have the dihydropodines like amalopene nidapine these primarily dilate arteries they reduce blood pressure can improve coronary blood flow so they increase oxygen supply they're typically added as second line therapy often combined with beta blockers

makes sense what about ranolazine seems a bit different

ranolazine is interesting it works by reducing calcium overload in the heart muscle during eskeeia it inhibits the late sodium current it's generally used as add-on therapy or maybe if other agents aren't tolerated well. One thing to watch with ranazine is potential QT prolongation on the ECG. So use it cautiously especially if the patient is on other drugs that also prolong the QT interval.

IVine you mentioned it briefly.

Ivabberdine. Yeah. It inhibits a specific current the if current in the heart sinus node to slow the heart rate down. It's approved in Canada for certain heart failure patients. Its role in stable angina is generally limited to patients who also have heart failure. A big trial signify showed no real benefit in stable CAD patients without heart failure. So it's not a go-to for typical stable angina. And just to round it out, remember nicarandil and tratazidine. They aren't approved here in Canada for stable angina.

That's a fantastic rundown of the angina prevention drugs. But as you said, managing stable angina isn't just symptom relief. It's about long-term protection. How do we use pharmarmacology to tackle those big risks, cardiovascular deaths and non-fatal MI?

Right. This is the other major pillar of treatment. We need to stabilize those coronary plaques and prevent clots from forming which is what triggers heart attacks. The evidence here is really strong for three main groups. Anti-ippidemic therapies, anti-thrombotic agents and RAAS inhibitors.

Okay, let's start with anti-ipidemics. Statins I assume.

Statins are definitely the cornerstone of anti-pipemic therapy. HMG COA reductase inhibitors. Their benefit goes beyond just lowering LDL cholesterol. They also seem to improve endothelial function, the health of the artery lining. Big trials like TNT really drove this home. They showed that higher intensity statin therapy like a tovvisatin 80 milligrams significantly reduced major cardiovascular events compared to lower doses in stable CAD. So current Canadian guidelines push for aggressive LDL targets aiming for below 1.8 millol or at least a 50% reduction from baseline for these high-risisk patients. And if statins alone aren't enough to reach those goals, we now have evidence for add-on therapies like aetami the PCSK9 inhibitors alcomaboomab and icosapent ethyl. These have all shown further reductions in eskeemic events especially in higher risk folks.

Aggressive lipid lowering is key. What about anti-thrombotics, anti-platlets and anti-coagulants.

Okay. Anti-thrombotic agents. Anti-platlet therapy is pretty much standard of care for almost all stable angina patients unless there's a strong contraindication. Lowdos ASA aspirin typically 80 to 160 milligrams daily significantly cuts the risk by about 30% of cardiovascular death MI or stroke. It's foundational. Clapig girl is generally reserved for those who truly cannot tolerate ASA maybe due to allergy or severe GI issues unless of course they've had a recent acute coronary syndrome or PCI where it's often part of dual antiplatlet therapy for a time. Teagriller specifically the 60 milligram twice daily dose from the Pegasus Timmy 54 trial showed a small but significant benefit in reducing events for high-risisk patients after an MI when added to ASA. But importantly, it comes with about a 1% absolute increase in major bleeding. So it's a consideration for secondary prevention but requires careful patient selection.

So mostly ASA sometimes copidogeral maybe to kagral or postMI. What about combining anti-platlets and anti-coagulants?

Ah that's the dual pathway anti-thrombotic therapy concept really highlighted by the compass trial. This involved combining lowd dose ASA 100 milligrams daily with a very low dose of the anti-coagulant river roxaban 2.5 milligrams twice daily. Compared to ASA alone this dual pathway significantly reduced the combined outcome of CB death MI or stroke. Even all-c causeed mortality was lower. However, and this is a big hono, however, it also significantly increased major bleeding roughly from 1.9% to 3.

1% though importantly not fatal bleeding. So, the decision to use this dual pathway strategy is highly individualized. You have to weigh that potential benefit against the bleeding risk and consider cost too. It's not for everyone.

That trade-off is crucial. Okay. Lipus thrombotics. What about ACE inhibitors? You mentioned RA inhibitors,

right? AC inhibitors or ARBs. If ACIs aren't tolerated due to cough, For example, these aren't just for blood pressure. They seem to have direct anti-semic effects, maybe decreasing sympathetic tone, reducing afterload, improving coronary flow. And importantly, large trials, notably the hope trial with ramipril showed they prevent major cardiovascular events in stable anggina patients even if they don't have heart failure or lvystolic dysfunction. Ramapril 10 milligrams alien hope reduce the relative risk of CV death, non-fatal MI or stroke by about 20% in the angina subgroup. So they're strongly considered especially if the patient also has hypertension. If they get the cough, an ARB is a reasonable substitute. As for other potential plaque stabilizers like anti-inflammatory agents, methtotricate, cultine, kakunamab, the results from trials have been mixed. Their role isn't really established yet for routine care in stable angina.

That's incredibly insightful on risk reduction. Now, flipping the coin, what should we be wary of? Are there specific agents we should definitely avoid or use only with extreme caution?

Absolutely. Two major classes really stand out. Firstly, systemic hormone therapy for post-menopausal women. It should not be prescribed if they have CAD. Studies consistently show it increases the risk of venus throbo embolism, blood clots, and provides zero benefit, maybe even harm regarding major adverse cardiovascular events and mortality. Just don't do it for cardiovascular protection. Secondly, Calobex 2 inhibitors and most non- selective NSAs common pain relievers. They are known to increase the risk of vascular events, heart attack, stroke. So, if a patient absolutely needs an NSAI for say severe or arthritis impacting their quality of life. The rule is use the absolute lowest effective dose for the shortest possible duration and weigh those risks carefully.

Crucial safety messages there. Hormone therapy and NSAIS be very cautious. We touched on treating modifiable risk factors earlier as a key goal beyond just the heart meds. Can you elaborate a bit more on the non-medation strategies for these?

Certainly that holistic approach is fundamental. You can't overstate it. Smoking sessation is probably the single most impactful intervention a patient can make in encouraging quitting and really supporting them with pharmacologic aids if needed. Nicotine replacement, bipion, verenocline. It dramatically cuts mortality and cardiac events. It's huge.

Number one priority, right?

Absolutely. Then aggressive management of coexisting conditions like hypertension and diabetes is also paramount. Get those numbers under control. And specifically for diabetic patients who already have established atheroscllerotic vascular disease, so CAD, peripheral artery disease, etc. Two classes of diabetes meds have really emerged. The SGLT2 inhibitors and the GLP-1 receptor agonists beyond lowering blood sugar, they've shown impressive benefits in actually reducing eskeemic complications, heart attacks, strokes, cardiovascular death in this population. So, they're now generally preferred agents after metformin for these specific patients. That's a major shift in practice.

That's a key update for diabetes management in CAD. Good to know. Anything that's not recommended, things people might ask about?

Yeah, definitely. Despite maybe past hype or common beliefs, large trials have conclusively shown no benefit for several supplements in patients with anggina. This includes things like folic acid, B vitamins, B6, B12, vitamin E, vitamin C, betaarotene, and even omega-3 fatty acid supplements for this specific indication. They just don't prevent cardiovascular events in this setting.

Similarly, EDTA chilation therapy also found ineffective in rigorous trials. So, best to advise patients to save their money and focus on the proven therapies.

Stick to the evidence. That's vital. Okay, let's try to bring all this together now. are some practical pearls. Those invaluable therapeutic tips for clinical success, especially things our PBC candidates should lock down.

Okay. Yeah, let's get practical therapeutic tips. First, titration for those heart rate lowering anti-angals, beta blockers, deltas, verapamil, you generally titrate the dose to achieve a resting heart rate target. Usually aiming for somewhere between 50 and 60 beats per minute. For the dihydropodine CCBs like amladepine or nifotine, you titrate more based on symptoms. relief versus side effects like ankle swelling. Maximize the benefit, minimize the adverse effects.

What if someone has a slow heart rate to begin with?

Good question. If a patient has resting brady cardia, but you still feel a beta blocker is strongly indicated maybe postmi, you could consider agents with what's called intrinsic sympathomimedic activity or isa

like asopalol or pendalol. They tend to lower the resting heart rate less dramatically than other beta blockers. It's an option.

Combining agents. Any tips there?

Yes. If you're going to combine a calcium channel blocker with a beta blocker. The general preference is to use a peripherally acting dihydroparodine CCB like amloopene. If you do choose to combine verapramil or diltasm the non-dihydroparodines with a beta blocker, you need really close monitoring of heart rate and avodal function because both drug classes slow conduction there. Risk of heart block goes up.

Okay. And ACE inhibitors,

right? We mentioned the cough. If a patient develops that nagging dry cough from an ACC inhibitor, that you've prescribed for vascular protection. Switching to an ARB and angotensin receptor blocker is a totally reasonable and effective alternative. They provide similar benefits without the cough usually.

What about really high-risisk patients?

For your very high-risisk patients, maybe extensive CAD, multiple coorbidities. Don't be afraid to consider a more aggressive multi-prong secondary prevention strategy. This might mean thinking about things like dual anti-pipid therapy, statin pluses or PCSK9I. Maybe dual anti-thrombotic therapy like ASA plus river oxaban carefully selected and an ACIRB really stacking the deck in their favor

and the basics

always the basics encourage annual influenza vaccination recommend appropriate COVID 19 and numaccoal vaccines based on guidelines and at every single clinical encounter review and promote medication adherence ask about side effects cost issues understanding it's absolutely foundational if they don't take the meds none of this works

these practical takeaways are absolute gold thank you now this raises is an important question for tying things together. We've referred to figure 1 and table two from therapeutic choices quite a bit. How exactly do these resources, the algorithms and the drug tables truly help someone, especially when they're prepping for an exam like the PEBC? What's their core function in your clinical toolkit?

Ah, they are absolutely central. Think of figure 1, the medical management of stable and ginopus algorithm as your strategic roadmap. It lays out a logical step-by-step approach. It shows you the flow, first line options, second line add-on therapies. It's not necessarily about memorizing a strict order of preference because choices depend on the patient, right? But it shows you the rational progression based on patient factors and contraindications. Using that figure helps you start thinking clinically, systematically like an expert would approach the problem.

So it's the thinking process. What about table two?

And then there's table two, drugs to treat stable angina. This table is like a super concentrated knowledge base, a cheat sheet almost, but a really detailed one for each key medication class.

It condenses critical info, drug names, maybe cost indicators, approved indications, typical dosages, crucial adverse effects to watch for, significant drug interactions, and really important clinical comments or pearls. Think about its value during an exam or even quick checks in practice. Need to quickly recall ranolysine's QT risk or ASA's bleeding issues or the specific warnings for beta blockers in asthma or that non-adocable nitrate-free interval. It's all there. It's your rapid, reliable reference for those key details you need for safe prescribing and for answering exam questions accurately. Essential resource.

This has been an incredibly thorough, really helpful deep dive into stable angina. Especially for our PBC candidates listening, we've covered so much ground from that foundational definition and its different faces to the critical goals of therapy, the essential diagnostic steps, those nuance pharmacologic and non-farmacologic choices, and yeah, those invaluable practical tips that really make a difference.

Indeed, and I hope listeners grasp that. Mastering these details, knowing how to navigate those algorithms, how to quickly pull key facts from drug tables, it doesn't just prepare you for an exam. It genuinely builds your confidence for providing effective and importantly safe patient care out there in the real world.

Absolutely. As you continue your studies, maybe mow over this thought and a patient with stable angina, how might their individual risk factors for bleeding? Maybe they're older, maybe they have kidney issues. How might that critically influence your choice between single versus dual anti-troic therapy? Even when both strategies might show some cardiovascular benefit on paper. It's that clinical judgment piece. Okay, before we wrap up, let's do a quick check of your knowledge of the multiple choice question. Ready? Which of the following instructions should be given to a patient taking sublingual nitroglycerin for acute angina? A. Take up to five doses every 5 minutes until pain resolves. B take the medication standing up to improve absorption. C. If discomfort persists for 5 minutes after one dose, seek immediate medical attention. Or D, headaches are sign of an allergic reaction and therapy should be stopped. Think about it that way. The correct answer is C. If one dose doesn't work within 5 minutes, it could be something more serious like an MI and they need urgent medical help. We really hope this deep dive has been incredibly helpful for your PBC preparation and beyond. Thank you so much for joining us on the deep dive. Keep exploring, keep learning.

سندروم کرونری حاد
Okay, let's unpack this. Imagine a patient walks into the emergency room right now. Uh, crushing chest pain. What's the immediate thought?

Yeah. What's that critical diagnosis everyone's thinking

exactly? Chances are it's acute coronary syndrome or ACS. Today, we're taking a vital deep dive into ACS.

We're specifically focusing on the essential details from the therapeutic choices chapter. Now, this deep dive is well absolutely crucial for Canadian pharmacist people. BC candidates.

It really is.

And our mission is simple. Cut through the complexity, give you concise, actionable knowledge, and hopefully some real peace of mind for your exams and future practice.

That's the goal.

And this deep dive is brought to you by the Pharma Board Group based on the CTC reference. So you know you're getting accurate, practical, and uh highly relevant insights.

And what's fascinating here, I think, is how these complex guidelines, these algorithms, they translate directly into critical, you know, often split-second decision-m in real time. In patient care, our aim isn't just to list facts. It's about connecting the dots, highlighting not just what to know, but really why it matters and what truly stands out for your understanding.

And we'll make sure the pace is clear, right? So everyone can grasp these critical nuances.

Definitely, we'll take our time.

So let's define our terms first. What exactly falls under that urgent umbrella of ACS?

Well, ACS is uh it's a broad term. It captures clinical symptoms that suggest acute moardial eskeeia. Think of it as a spectrum really on one end you've got unstable anggina UA and non-ST segment elevation myioardial inffection in stami

right

those two are often grouped together as non-ST elevation acute coronary syndromes or in stamps

and stance got it

and then at the most critical end the most urgent end we have ST segment elevation myioardial infarction which everyone knows is STEMI

STEMI and what's typically driving these events like at a fundamental level

so at its core the problem is usually an issue within the coronary arteries themselves. Uh most often plaque erosion or rupture and that can lead to a thrombus, a clot forming and obstructing blood flow to heart muscle.

When a patient presents with suspected ACS, time is heart muscle, right? That's the phrase.

Absolutely. Time is critical.

So, how do clinicians even begin to untangle what's happening? What are those initial critical steps?

That's right. Prompt and accurate assessment is paramount. It starts with a careful patient history, understanding the pain, its duration, any previous cardiac issues they've had.

Okay.

Then a thorough physical examination follows looking for signs of distress or say heart failure. And then we move to key lamb tests. Traropponin, for instance, is highly sensitive and specific for myioardial injury.

And that's our gold standard marker, isn't it? If traroponin is up, it's always a heart attack.

Well, not always. And that's a really critical insight actually. While tropparonin is our most reliable marker for myioardial injury, its very sensitivity means it pops up in other situ situations too.

It underlines a vital diagnostic challenge. Sorting out true eskeeia from other systemic stressors. So when you see a high troponin, your thought shouldn't just be MI, but more like okay, what's the whole story here,

right?

Tropponin can also rise in conditions like severe heart failure, pulmonary embolism, sepsis, even just critical illness generally.

Wow.

And here's a specific exam nugget for you. Biotin supplements. They can only interfere with some tropparonin assays leading to falsely low values.

Falsely low. Okay, that's definitely something to remember. Biotin

always something to consider. Yeah,

that's a great practical tip. So once we have some initial findings, how do clinicians quickly assess a patient's risk? Is there a fast reliable way to do that bedside?

Yeah, that's where tools like the TMI risk score become really indispensable.

It helps quantify that initial gut feeling, giving a rapid sense of the patient's prognosis.

So it's like a checklist

kind of. Yeah. Think of it. is a quick checklist. Each of its key clinical features things like being over 65, having three or more cardiac risk factors

like diabetes, hypertension.

Exactly. Known coronary stenosis, recent aspir angina episodes in the last 24 hours, elevated cardiac markers or ST segment deviation on the ECG. Each one counts for one point each,

right?

And the higher the total score, the higher the predicted risk of adverse outcomes like death or recurrent MI down the line. So it's not just for diagnosis, but it helps guide the urgency of treatment too. Right there at the bedside.

Exactly. It helps stratify risk quickly.

Yeah.

And while TMI is widely used, it's worth just briefly mentioning the Gracie score.

Okay.

It's a more comprehensive tool. It's web- based and it actually provides even better discrimination for predicting mortality both short-term and longer term in ACS patients. It digs into a few more parameters.

Good to know there are options. All right, let's pivot from diagnosis to action now specifically for you and STEMI first. Once we know what we're dealing with. What are the big therapeutic goals and what are those immediate non-drug steps?

Okay, for you and STEMI, the main goals are pretty clear. We need to decrease mortality and complications. We need to reduce the eskeeia, the lack of blood flow, and prevent any further myioardial injury.

Makes sense.

Non-farmacologically, this often begins with bed rest while the eskeeia is active. Once things stabilize, patients can gradually mobilize. And for those high-risisk patients, continuous ECG Monitoring is crucial.

Why the monitoring?

To watch for arhythmias or any further ST segment shifts that might indicate worsening eskemia or an evolving MI.

Gotcha. Now, this is where it gets really important for us pharmacists. Let's talk medications. The choices can be quite nuanced, right?

Yeah.

What are we reaching for first usually to provide symptom relief?

Right. This is where understanding the drug classes is critical. Initial symptom relief for you and Stanga often involves nitrates, typically sublingual nitroglycerin first. Okay. Nitro spray or tablet.

Exactly. But here's a huge point for your practice and definitely for exams. Those contraindications are absolutely vital to remember. If a patient has used selenophil or vardinophil within the last 24 hours or tadalapil within 48 hours, nitrates are a no-go.

Big no-go. Why again?

Because of the risk of profound life-threatening hypotension when you combine them,

right? Those PD5 inhibitor interactions always tricky. Okay. So, after nitrates, what's next for managing symptoms and protecting the heart muscle? blockers. They're a cornerstone therapy. They should be started as soon as possible in pretty much all patients unless they have contraindications like severe paradic cardia, signs of shock or maybe severe reactive airway disease.

And how do we use them?

The dose is carefully titrated up to achieve target heart rates usually around 50 60 beats per minute resting. And in cases where the pain is ongoing, they can even be given introvenously initially for faster effect.

Okay. What about calcium channel blockers? Where do they fit into the UN stem? Good question. Calcium channel blockers or CCBs are generally reserved for ongoing symptoms when patients are already on max doses of beta blockers and nitrates or if beta blockers just aren't tolerated at all.

So not first line usually.

Not usually. No, they're also key in cases of variant angina. That's angina caused by coronary artery spasm.

Ah okay.

But a really vital distinction here the nondihydropodian CCBs like deltasm and verapamil You need extreme caution combining those with beta blockers.

Why is that?

Risk of excessive slowing of the heart rate, severe bradic cardia or worsening left ventricular function and definitely definitely avoid immediate release knifetipene.

Immediate release nephetipene. Why?

It's been associated with an increased risk of stroke in this setting. So stick to the longer acting formulations if you need a dihydrop.

Okay, that's a serious red flag to remember. Immediate release nettine is out. What about ACE inhibitors? When do they come into play?

ACE inhibitors are crucial. for reducing mortality particularly in patients who have evidence of left ventricular systolic dysfunction. So reduced ejection fraction or signs of heart failure or diabetes or if they've had a recent MI.

So specific groups benefit most.

Yes. And ideally they should be started within 24 hours in these high-risisk groups. ARBs are the alternative if ACEs aren't tolerated.

Now let's talk clots. Preventing those crucial clots from forming are getting bigger. What's the strategy for anti-coagulation and anti-platlet therapy in and STEMI

absolutely essential part of management for anti-coagulation. Hepins are a cornerstone and oxiparin which is a low molecular weight hepin or LMW is generally preferred over unfractionated hepin UFH.

Why is an oxiparin preferred?

Mainly because it has a more predictable anti-coagulant response and it's easier to administer subcutaneous injections versus an IV infusion that needs monitoring.

Easier. Okay. Any exceptions?

Yes. The big one is significant renal dysfunction. If the creatinine clearance is below 30 molan, then unfractionated hepin is generally the safer choice because it clearance isn't kidney dependent.

Good point. Renal function matters. Any other anti-coagulants?

Fontaranex is another option. It's an indirect factor as a inhibitor. It's also effective and notably it seems to have a lower bleeding incidence compared to an oxiparin in some studies.

Lower bleeding. That's good. Okay. And for antiplatlets, we know ASA is key.

ASA is foundational. Yes. Started promptly, continued longterm. Usually 81 milligram daily long-term after an initial loading dose but it's typically combined with a second antipllet agent

and that's where the P2Y12 inhibitors come in clapitol tagrreller prashugril

exactly clidal was the first big one shown to provide benefit when added to ASA significantly reducing adverse cardiac events

but there's a catch with clapidogil right the genetics

yes that's a key nuance its effectiveness can be diminished in patients who are poor metabolizers due to certain genetic vari in the CYP2C19 enzyme which is needed to activate the drug.

Do we test for that routinely?

No. Routine genetic testing isn't currently recommended across the board, but it's an important factor to consider. If a patient isn't responding as expected or if they have a spent thrombosis despite being on clapadogil

okay so that led to the newer more potent options like prashagil and teagural what makes them different

precisely prugil is more potent than clopedogil but that potency comes with a significantly increased risk of bleeding

more bleeding risk. especially in older patients, those with low body weight or anyone with a prior history of stroke or TIA. It's actually contraindicated in patients with prior stroke IIA. So, its use is generally more restricted, often considered in higher risk patients undergoing PCI, particularly if they're getting a stent and are at high risk for stent thrombosis.

So, careful patient selection for proagril. What about teagur?

Togagler is also more potent than clapadigril and it has an advantage in that it doesn't require metabolic activation. So its onset and offset are faster and perhaps more predictable.

No activation needed,

right? Studies like Plato showed it led to lower rates of cardiovascular death, MI or stroke compared to Clapopil.

That sounds good. Downsides.

It does come with an increase in non-annabi related major bleeding. And a fairly common side effect is dysmia or shortness of breath which can sometimes lead to patients needing to switch therapy.

Dysmia. Okay. Wow, that's a lot of detail on the antiplatlets, but it's clearly critical.

So pulling this together for pharmacists especially for exams any practical therapeutic tips to consolidate this unmi management

absolutely a crucial tip remember that standard long-term ASA dose is 81 milligrams daily get that loading dose right initially but it's 81 milligrams long-term

81 millig daily check

and know those holding times for non-urgent bypass surgery this comes up clapidogeral or dicagular should ideally be held 5 days prior pressure needs even longer 7 days.

5 days for clapigel to coaguler, seven for paragrow. Got it. Why the hold?

To reduce the risk of major bleeding during and after the surgery. That distinction and holding times is really important for patient safety around CBD.

Okay. Very practical. Now, let's shift gears completely to STEMI ST elevation MI. This is truly a medical emergency, isn't it?

Absolutely. Time is critical here. Even more so than NT STEMIs.

Okay. The goals must be even more immediate, more critical.

They are. We're aiming to decrease mortality obviously, but also contain the infar size limit, the amount of heart muscle damage, salvage as much myioardium as possible, and crucially quickly reestablish patency or openness of the infar related artery, get the blood flowing again fast.

And the initial investigations, still history, ECG, traropponin,

yes, but with even more urgency, rapid targeted history, stat ECGs often repeated every 1530 minutes if the first isn't diagnostic, but suspicion is high. And baseline traropponin though treatment decision s for STEMI often can't wait for the tronin result if the ECG is clear

right the ECG changes are key so how do we achieve that rapid reestablishment of blood flow what's the gold standard approach

primary perccutaneous coronary intervention or PCI angoplasty and often stenting that's the preferred firstline therapy for most STEMI patients

PCA but there's a time window right

yes a critical one yeah the goal is to get the patient from first medical contact like paramedics arriving to the device being used in the kath lab in 90 minutes or less.

90 minutes FMCA to device.

Exactly. That's the ideal scenario, especially if they can get to a hospital that does a lot of PCIs.

What if PCI isn't immediately available, say in a more rural setting or if transport takes too long? What's plan B?

Good question. If PCI isn't feasible within about 120 minutes or 2 hours of that first medical contact, then a phiccoin invasive strategy is recommend.

Phicinvasive meaning drugs first.

Yes, it involves giving prompt fibbronolytic therapy clot busting drugs as the first line. approach to open the artery chemically

fibbronolysis and there's a time goal for that too.

Absolutely. The goal is a door to needle time from arrival at the hospital to starting the fibbrronolytic infusion of 30 minutes or less.

30 minutes door to needle

right and it's most effective if it's given within the first few hours ideally within 6 hours of symptom onset. After fibbronolysis patients are typically transferred to a PCI capable center anyway for angography and potential rescue or routine PCI later.

Okay. Okay, that makes sense. Now, are there significant pharmacologic differences in managing STEMI compared to ENT STEMI that our listeners really need to zero in on?

Yes, there are definitely some key distinctions to know

like what?

Well, for anti-coagulation with fibbronolytics, introvenous unfractionated hepin is typically administered. An occipin has shown superiority with some fibbronolytics like tenectto but needs caution in the elderly or those with renal impairment.

Okay, what else? ASA is still key presumably.

Oh, absolutely. ASA is vital. Loading dose then daily continued longterm and maybe consider a PPI alongside it if the patient has a history of GI bleeding.

Right. Beta blockers too.

Yes, beta blockers are still recommended usually started orally within 24 hours once the patient is hemodynamically stable. We titrate to that resting heart rate of 50 60 BPM similar to NTEMI.

Okay, here's where I suspect a big difference lies.

Calcium channel blockers. You mentioned avoiding one earlier.

Exactly. This is crucial. Unlike you and STEMI, calcium channel blockers are generally not recommended routinely in STEMI.

Not recommended. Why?

Because studies have suggested they might actually increase morbidity and mortality in the post STEMI setting, particularly the short acting ones. They're only used very cautiously, maybe for persistent eskemia after reprofusion or for rate control and atrial fibrillation if beta blockers are absolutely contraindicated and there's no heart failure.

So a very limited role if any. What about nitrates? Are they used differently in STEMI?

Yes, also used more selectively. Not routinely given to every STEMI patient. like they might be for initial and STEMI pain. In STEMI, nitrates are generally reserved for patients with persistent or recurrent eskeeia or if the patient has complications like a large anterior MI, hypertension or signs of heart failure and avoided entirely in suspected right ventricular MI or severe hypotension.

Got it. More selective use of nitrates. How about AC inhibitors in those MRAs you mentioned?

AC inhibitors are routinely recommended post stemi for almost everyone. Ideally started within hours assuming no contraindications. They reduce mortality and remodeling. They can often be continued indefinitely.

So standard of care post STEMI

pretty much ARBs are the alternative for AC intolerant patients especially those with heart failure or LV dysfunction.

And then the mineralid receptor antagonist MAS like spironolactone or epernomanel those are important additions.

Maybe you add those

for patients who already have an LD ejection fraction under 40% and either have symptoms of heart failure or diabetes provided they are already on an ACE inhibitor and a beta blocker.

So specific criteria again,

yes, they've been shown to further reduce mortality in that group, but you absolutely have to monitor potassium levels closely for hyperc calmia,

right? Potassium monitoring is key with MRAS. And one quick clarification, antiplatelets in STEMI if they get fibonolytics.

Ah, good point. For STEMI patients treated with fibbronolysis, clapidogeral loading dose than daily dose is typically admin ministered a presentation along with SK teagriller is generally preferred if primary PCI is the strategy.

Okay. Clap girl with aolytics. Got it. Beyond the acute management, what are some of the common complications we need to keep in mind that can happen after a STEMI?

Yeah. Unfortunately, STEMI can lead to several complications. Things like recurrent eskeeia or reinfarction, heart failure developing or worsening, various arhythmias, both atrial and ventricular

dangerous arhythmia

can be. Yes. Like ventricular tacicardia or fibrillation. And then Y much rare but absolutely devastating are the severe mechanical complications

like what

things like a rupture of the papillary muscle leading to acute mitral regurgitation or a ventricular septile rupture a hole between the ventricles these are surgical emergencies.

Wow. Okay. Definitely things to be aware of. Now this raises an important question. How do we handle ACS in special populations? Pregnancy or breastfeeding comes to mind. That sounds like a unique challenge.

It absolutely is. And while care ACS in pregnancy seems to be increasing slightly. Management must always be collaborative. You need the obstetric team and the cardiovascular specialists working closely together.

Makes sense. What about medications?

Well, some are generally considered safe. ASA clapidal is usually the preferred P2Y12 inhibitor if needed. Unfractionated hepin, low molecular weight hepin, beta blockers, and nitrates can generally be used.

Okay. What's contraindicated?

Critically, ACE inhibitors, ARBs, and statins are all contraindicated due to to the risk of harm to the fetus. Terraogenicity,

ACEs, ARBs, statins out in pregnancy. What about reprofusion for STEM?

Primary PCI is definitely the preferred treatment for STEMI during pregnancy as it avoids the systemic effects of fibonolytics. Litics might be considered as an alternative only if PCI isn't readily available and the maternal benefit outweighs potential risks.

Okay. PCI preferred. And for breastfeeding mothers, similar considerations.

For breastfeeding mothers, the workup for ACS shouldn't be delayed. Medication wise, ASA, UFH, LMW and most beta blockers are generally considered safe

safe for breastfeeding

generally. Yes. However, data is limited for many other cardiovascular meds used in ACS like some antiplatlets or ACE inhibitors. So sometimes discontinuing breastfeeding might be necessary to prioritize the mother's treatment and health outcomes. It always a careful riskbenefit discussion with the patient.

A very complex situation. This has been incredibly detailed and practical. To maybe summarize some overarching therapeutic tips for our PBC candidates. What are the absolute musters from all this?

Okay, let's boil it down. Beyond those critical time goals, door to needle, A30 men for luittics, FMC to device AD men for primary PCI, remember specific scenarios like for right ventricular infarks, avoid nitrates and diuretics, use fluids, maybe inotropes to treat hypotension instead.

Right ventricle, no nitro. Got it.

Also, consistent early administration ideally within 24 for hours of beta blockers and ECE inhibitors postMI is crucial. Titrate them carefully.

Early beta blockers and ACEs.

Yes. And a practical tip for patient comfort, especially right after the MI, consider stool softeners to prevent straining which can stress the heart and maybe short-term anxolytics if needed for significant immediate postMI anxiety.

Good practical points.

Finally, and this may be the most important study tip, really know your algorithms like figure one for you on STEMI and figure two for STEMI and the references and become familiar with a comprehensive tables like table two covering dosages, side effects, interactions. They're invaluable resources for pulling it all together for exams and practice.

Fantastic summary. We've covered a huge amount today really from diagnosing ACS, navigating those complex therapeutic choices for both N STEMI and STEMI and even touching on critical special considerations like pregnancy. This deep dive hopefully gave you the most important nuggets from the therapeutic choices chapter, helping you feel genuinely well informed and uh maybe a bit more confident. Hope so.

So, here's a thought for you, the listener, to mull over. How does really understanding these specific drug interactions like we discussed with nitrates and PTE5 inhibitors or the nuances between antiplatlets? How does that knowledge directly translate into preventing real harm, preventing adverse outcomes in a busy everyday pharmacy setting? It's more than just memorizing facts for an exam, isn't it? It

really is. It's about patient safety.

Remember, this deep dive was brought to you by the Pharma Board Group based on the CTC reference. Okay, before we wrap up, here's a quick multiple choice question to test your knowledge based on our discussion. Based on our discussion regarding the management of acute coronary syndromes, which of the following medications is a contraindication for the use of nitrates in patients with unstable angina or nmi? Is it a metiprol, b selenophil, c clopidigrol, or d aspirin? Take a moment to think about it. Which one should make you stop and say hold on no nitrates? The answer of course is B selenaphil. Due to that at risk of significant potentially life-threatening hypotension. Remember, nitrate should not be used if selenaphil or vardmophil were taken within the previous 24 hours or tadalapil within the previous 48 hours.

Absolutely crucial point to remember. Keep diving deeper into your studies everyone. That critical thinking, that precise application of this knowledge, it will serve you exceptionally well both in your exams and more importantly in your future practice.

We look forward to our next deep dive with you.

نارسایی قلبی
Welcome to the deep dive. We focus on cutting through the noise to give you those critical actionable insights. And today, well, this one's specifically for you, our Canadian pharmacist PBC candidates. We really get the challenge you're facing, mastering complex topics like heart failure for your boards. Our mission today, honestly, it's about providing some peace of mind. We want to make sure you don't miss anything absolutely crucial for the exam and, you know, just as vital for your confidence when you're actually practicing. So, yeah. Today we're diving deep into heart failure. We're pulling out the essential bits from that key chapter in your text, therapeutic choices, medication algorithms, those really important tables, and uh practical tips that actually make a difference. This isn't just a summary. Think of it as a curated session.

That's exactly right. And just so you know where this is coming from, this deep dive is brought to you by the Pharma board group. It's specifically based on the therapeutic choices reference, the CTC. So you can be confident the information is solid and well directly relevant.

Absolely. Absolutely. And look, we know many of you might not be native English speakers, so we're going to keep the pace clear, easy to follow. We want every detail to really uh land properly. So, let's unpack this important topic together, taking our time. Okay. So, every patient walking into the pharmacy is, you know, a unique puzzle, but when it comes to heart failure, just understanding what it is, not just a diagnosis, but like a dynamic syndrome, that seems like the right place to start our deep dive. How do we first think about heart failure? or HF.

That's a great starting point. Yeah, HF isn't just one disease. It's um a complex clinical syndrome. Picture a patient coming in with say shortness of breath, that's dispa, maybe some fluid retention like swollen ankles, maybe a cough, and just feeling tired all the time. What makes it heart failure is when those symptoms line up with actual structural or functional heart disease. And that's often backed up by uh highriotic peptide levels or clear signs of congestion.

Right? So, it's a syndrome, a whole collection of things, not just one neat label. What's the bigger picture then for us as future pharmacists?

What's really important to grasp is how dynamic it is, how it progresses. Patients might feel stable for a while, but HF symptoms can definitely fluctuate. And even with all the advances we've made, its prevalence is actually increasing globally, mostly because populations are getting older. This makes it a huge contributor to well, morbidity, mortality, and health care costs. Just to give you an idea, annual mortality rates can range anywhere from 6% to maybe 25%. It really underscores how serious this is.

Wow. 6 to 25%. That definitely puts the impact into perspective. Yeah. Okay. Let's talk classification because, you know, for a pharmacist looking at a patient's chart trying to figure out the treatment plan, that lift ventricular ejection fraction, LVEF, that's kind of the hinge point, isn't it?

It absolutely is. LVEF is how we often sort HF patients and it really guides a lot of our therapy choices.

So, let's walk through those main types. Maybe starting with the one we've uh traditionally focused on most.

Sure. First up is heart failure with reduced ejection fraction. or HFR EF. That's defined as an LVF of 40% or less.

Basically, the heart's pump function is down and the left ventricle is often bigger, dilated. Historically, about half of HF cases fall into this bucket. And yeah, most of the big clinical trials were done in this group.

Okay. HFREF, LVF less than or equal to 40. Got it. And then there's the other side of the coin where the LVF looks well relatively normal.

Exactly. That's heart failure with preserved ejection fraction or HFPF. Here the LVF is 50% or higher. The problem isn't so much the pumping out but rather how the heart relaxes and fills its abnormal myioardial relaxation.

The left ventricle isn't dilated and you might see things like concentric remodeling or a bigger left atrium. HFPF uh tends to affect older patients, more women and folks with obesity, hypertension, aphib, sleep apnea, diabetes. Diagnosing it can be trickier which, you know, makes managing it tough too.

And there's those newer classifications popping up too, right? Just briefly.

Yeah. But briefly, there's HF with mildly reduced ejection fraction or HFMEF, that's LVEF between 41 and 49%. And then HF with improved ejection fraction, HFMPF, that's for patients who started with HFREF, but then their LVF got significantly better. These just show how HF can change over time.

Okay, so we have the definitions down, but when a patient is actually in front of you or you're looking at their profile, what are those specific red flags, maybe beyond just general fatigue or swelling that really scream heart failure to a pharmacist and What common things should we watch out for that could actually make their HF worse?

That's super important for assessment. Beyond the usual signs, look for more specific things like uh bendopnia, that's getting short of breath, just bending over, or an elevated jugular venus pressure, JVP, which signals fluid overload. A third heart sound, S3, that's a classic sign, too. Now, for the pharmacist eye, table four in your reference, it's not just a list. It's like your early warning system. It points out things that can make HF worse. Non-adherence to meds or diet. Huge. infections absolutely and critically certain drugs. We're talking medications that cause sodium and fluid retention like NSAIDs, thazolid, adion also negative inotropes. Think non- dihydropiritine calcium channel blockers like deltasm, verapamel, and most antiarithmics. Recognizing these can honestly be the difference between stability and an ER visit.

Okay, so we suspect HF based on those signs and maybe potential triggers. How do we actually confirm it? What are the really crucial first tests that nail down the diagnosis? Right. So, while a good history, physical exam, and standard labs are all foundational, the echo cardiogram is absolutely essential for all patients with suspected heart failure. It's the key test. It shows ventricular size, how well it's pumping the LVF, and checks the heart valves. Without it, you're really just guessing.

And what about those naturic peptide tests like BNP or NT Probnp? Where do they fit in?

These tests, you'll see them in table 5. They're incredibly useful, especially if the diagnosis isn't totally clear. They help us rule pull in or rule out HF. For example, a BNP below 100 PGML makes HF pretty unlikely. But if it's over 400 PGML, then HF is very likely. Those cut offs are handy to remember.

All right, so we've got a clearer picture of what HF is and how it's diagnosed. But let's pivot now to the why. When we're managing a patient with heart failure, what are the big goals driving every decision we make about their treatment?

Ultimately, the goals are kind of twofold. First, and this is critical, we want to reduce mortality, keep people alive longer, and reduce morbidity, which really means preventing those awful HF hospitalizations and flare-ups. Second, and just as important for their day-to-day life, is improving their symptoms, helping them be more active, boosting their exercise tolerance, and just generally improving their quality of life. It's about quality, not just quantity.

And as pharmacists, even before we jump to the meds, what are those foundational non-drug strategies we should be talking to patients about?

These are absolutely the bedrock. Patients need to manage other conditions. CAD diabetes, high blood pressure. They have to avoid those trigger factors we mentioned from table four. Lifestyle is huge. Moderate regular activity if they're stable, strict sodium limits like less than 2 to three grams a day and limited alcohol max one drink a day or none at all if it's alcoholic cardiammyopathy. And something really specific you should advise daily weight monitoring.

Tell patients, call us or your doctor if you gain half a kilogram a day for a few days straight or 2 kg in just 3 days. That's often the very first sign of fluid building up.

Oh, and keeping up with vaccinations, flu, numaccoal, COVID, that's really recommended, too.

Those non-drug steps are clearly vital. But sometimes patients need more help. Before we get into the powerhouse medications, what advanced tools might come into play for more severe cases?

Yeah, for more advanced situations, we start thinking about device therapies. Things like implantable cardioverter defibrillators, ICDs, or cardiac recynchronization therapy, CRT. Sometimes even left ventricular assistant devices, LVADs, and then there are surgical options like revascularization or even heart transplantation for specific patients. These definitely pave the way for the medications which are often the main pillar of therapy. And what's really interesting now and it's a big shift in the guidelines is this push for early initiation of quadruple therapy. It's the new standard really for managing HFREF. It means starting four key drug classes pretty much right away.

Okay, quadruple therapy. So the goal then is to start all four. That's an AR NI or an ECE inhibitor or an ARB plus a beta blocker plus an MRA plus an SGLT2 inhibitor and then carefully titrate them up to the target dose or whatever the patient can tolerate ideally within what 3 to 6 months. But you said there's no prescribed order for starting them feels flexible but maybe a bit daunting. How do we as pharmacists decide where to begin if there isn't a set ABC? What's your insight there?

That really comes down to clinical judgment. While there's no strict order, you look at the patient in front of you. What are their symptoms? like right now, what's their blood pressure, renal function,

potassium level? So, for instance, if someone's really congested, you might adjust their diuretic first, maybe alongside starting an ACI or ARNI to manage volume. If their heart rate's high and blood pressure allows it, maybe a beta blocker is a good early step. The key is to get something from each class going as soon as you can and then systematically work on optimizing. Don't feel like you have to max out one drug before starting the next.

Okay, let's dive into each of these. core classes focusing on the practical stuff you need to know starting with a inhibitors and ARBs

right their role seems clear in improving symptoms cutting down hospitalizations MIS death but what are the key monitoring points for pharmacists what do we really need to watch vigilance is definitely key you need to check their serum creatinine potassium and blood pressure usually about 7 to 14 days after starting or changing the dose and here is a critical point for exams and practice it's nor normal, even expected to see serum creatinin go up by maybe 30%. That's generally okay. The main risks you're watching for are hypercalemia, hypothacium, and anodema, that's swelling. Be extra aware that angodma is more common in patients who identify as black, those with a history of drug rash or older folks. If someone gets that ACE inhibitor cough or angiodma, ARBs like candaceartin or sartin are good alternatives, but still keep an eye out for angodma even though it's less common with ARBs. Okay, next up, the AI. Right now, that's the basartin. vitrol combo on tresto.

Yeah, that mechanism is different and the big paradigm jackf trial showed it was better than an elilapal for reducing CV death and HF hospitalizations, but you mentioned a mandatory 36-hour wash out when switching from an AC inhibitor. That sounds critical. Have you seen problems when that's missed? What's the real risk?

Oh, it's absolutely critical. And yes, problems definitely happen if that wash out is skipped. The risk is a significantly higher chance of angiodma. Those 36 hours are non-negotiable. Really, another key point, if a patient's on an ARNI regular BMP levels aren't useful anymore.