Cardiology
Expert discussions on heart failure, arrhythmias, interventional procedures, and cardiovascular risk management.
Recent Discussions
How do you recommend mitigating the risks of using beta blocker and clonidine therapy in combination for management of hypertension?
Beta blockers vary in lipophilicity, which affects blood-brain barrier permeability. Propranolol and metoprolol readily cross the blood-brain barrier, while other beta-blockers like nebivolol do not. The CNS side effects of fatigue, depression, and insomnia are more likely to worsen if using a lipop...
What is your approach to GDMT uptitration (particularly dosing for ARBs/ARNIs/MRA) if there is further evidence of renal dysfunction, especially in situations with worsening AKI on CKD?
Titration of RAAS inhibitors in the setting of AKI on CKD is challenging. First, look at the patient: if they have an increase in Cr after an increase in the RAAS inhibitor but no/stable HF symptoms and appear euvolemic on examination, then I will decrease diuretic therapy and see if the Cr improves...
In patients with post-MI LV thrombus which resolves after 3-6 months of anticoagulation, would you consider surveillance imaging for thrombus recurrence if there is persistent apical akinesis?
I think the key word here is akinesis (or dyskinesis); effectively, an immobile segment of myocardium gravitationally farthest south of the ‘northward’ flow of blood across the aortic valve. This effectively allows for stasis in an injured and immobile region... two of the three components of Vircho...
What is the most updated consensus regarding the use of pill in the pocket oral anticoagulation in paroxysmal atrial fibrillation, and populations of patients who are most likely to be considered for enrollment in clinical trials?
I'm not sure that there is a consensus. The best available large trial data would recommend anticoagulation based on a CHADS2Vasc score of 2 or higher, while a score of 0 patients could be off anticoagulation, and if the score is 1, patients would benefit from shared decision-making. For the CHADS2V...
Do you counsel patients to take antihypertensives at specific times of day to maximize efficacy or minimize side effects?
I counsel my patients to take antihypertensives in the morning. The only exception is the alpha-1 antihypertensives. I use them only as an add-on, to be taken at bedtime for two reasons: one is to avoid the blood pressure surge in the early morning hours, and two is to minimize orthostatic blood pre...
Would it be reasonable to begin considering GLP1 RAs or finerenone for patients with heart failure with recovered LVEF in light of recent trials such as SELECT and FINEARTS-HF showing some success in HFpEF and HFmrEF populations?
I reject the premise of the question. Patients with HFrEF who improve on medical therapy do not become HFpEF. The pathophysiology of these diseases are entirely distinct and it speaks to the limitation of EF as a categorical variable. HFrEF patients have cardiomyopathy that manifests over time as di...
Can a dihydropyridine calcium channel blocker (CCB) like amlodipine be prescribed in addition to a non-dihydropyridine CCB such as diltiazem or verapamil for treating hypertension?
Yes, with extreme caution. Diltiazem and Verapamil are CYP450 inhibitors, which can interfere with the metabolism of many medications (commonly statins and calcineurin inhibitors), but also can increase levels of nifedipine and presumably other dihydropyridine CCBs, like amlodipine. Diltiazem or ver...
For optimal GDMT for patients with HFrEF and co-existing ESRD, is there evidence to support the use of SGLT2 inhibitors and/or ARB/ARNI?
For patients with heart failure with reduced ejection fraction (HFrEF) and co-existing end-stage renal disease (ESRD), the use of sodium-glucose co-transporter-2 inhibitors SGLT2i and angiotensin receptor blocker/angiotensin receptor-neprilysin inhibitor ARB/ARNI therapies requires careful considera...
How do you approach caring for patients admitted with decompensated CHF, but who also exhibit hypotension and do not have overt signs of hypervolemia on exam?
This is a case where you might be concerned about the patient sliding into cardiogenic shock. Remember that in the context of chronic heart failure, cardiogenic shock tends to present more insidiously because these patients are typically compensated at low or borderline low cardiac output (Abraham e...
Is it reasonable to start de-escalating GDMT for patients with recovered LVEF following PCI for anterior STEMI, and if so, what class of medication would you consider stopping first?
This depends upon what is defined as "recovered" (TTE vs cardiac MRI), but I would be hesitant to de-escalate - wary of second "hits" and the natural history of LV trajectories (Lupon et al., PMID 30071987 - albeit the IHD cohort is not included here).Age and co-morbidities (younger - more "life yea...