Dr. Usman's Cardiology Notes

Contraindications of Digoxin Absolute Contraindications : ❶ Ventricular fibrillation ❷ Digoxin hypersensitivity Relative Contraindications : ① Acute MI ② Myocarditis ③ HOCM ④ Sick sinus syndrome ⑤ AV block (2nd- or 3rd-degree) without a pacemaker ⑥ WPW syndrome with AF Drug Interactions that Can Function as Contraindications : ☒ Amiodarone ☒ Dronedarone ☒ Verapamil ☒ Macrolides (e.g., clarithromycin) ☒ Itraconazole Conditions that Increase Risk of Digoxin Toxicity : ➠ Renal impairment ➠ Hyperthyroidism or Hypothyroidism ➠ Elderly or low body mass ➠ Electrolyte disturbances :  ➜ Hypokalemia  ➜ Hypomagnesemia  ➜ Hypercalcemia For more infographics keep visiting: drmusmanjaved.com Contraindications of Digoxin – A Detailed Clinical Guide Digoxin is one of the oldest and most widely used cardiac medications, particularly in patients with atrial fibrillation and heart failure with reduced ejection fraction (HFrEF) whose primary problem is symptomatic congestion despite optimal therapy. Altho...

  “Silent Threat: When Coronary Anomalies Turn Deadly — Understanding the Risk of SCD from Weird Heart Arteries” 🫀 What are anomalous coronaries? In a typical heart, coronary arteries arise from specific sinuses of the aorta and follow predictable courses. But in some people, there’s a congenital variation — a so-called Anomalous aortic origin of a coronary artery (AAOCA), or other Coronary artery anomalies (CAA). In AAOCA, a coronary artery arises from the “wrong” sinus of Valsalva. That misplacement often forces the artery to take a dangerous path — sometimes between the aorta and the pulmonary artery, or within the aortic wall (“intramural”).  Many of these anomalies remain silent and undetected for years. Indeed, population studies estimate CAA incidence between roughly 0.2 % and 1.2 %.  --- Why anomalous coronaries can cause Sudden Cardiac Death (SCD) 🔹 High-risk anatomy Not every coronary anomaly causes trouble — but certain “high-risk” variants do. Key danger fea...

  Hypokalemia: Diagnosis and Management Hypokalemiaypokalemia, defined as a serum potassium level below 3.5 mEq/L, is one of the most frequent electrolyte abnormalities encountered in clinical practice. Despite its frequency, it can be dangerous, predisposing patients to muscle weakness, arrhythmias, and even sudden cardiac death. Early recognition and appropriate treatment are essential. --- Why Potassium Matters Potassium plays a key role in: Maintaining resting membrane potential Neuromuscular function Cardiac conduction and repolarization Smooth muscle function Even mild hypokalemia can be potentially dangerous in patients with heart disease or those on digitalis. --- Classification of Hypokalemia Severity Serum Potassium Mild 3.0 to 3.4 mEq/L Moderate 2.5 to 2.9 mEq/L Severe Less than 2.5 mEq/L --- Clinical Features Symptoms Generalized weakness and fatigue Muscle cramps Constipation or ileus Polyuria and polydipsia Severe or Acute Hypokalemia Paralysis Rhabdomyolysis Life-thr...

Understanding LV Diastolic Dysfunction via Mitral Inflow Doppler: Mitral inflow Doppler patterns reflect LV diastolic function. Pulsed-wave Doppler at the mitral valve leaflets shows E (early filling) and A (atrial contraction) waves. Here’s how the patterns change: 1️⃣ Normal Filling: - E/A >1 - Deceleration Time (DT) <220 ms - Normal relaxation and compliance. 2️⃣ Grade I – Mild Dysfunction (Impaired Relaxation): - E/A <1 - DT >220 ms - Relaxation is delayed, atrial kick becomes dominant. 3️⃣ Grade II – Moderate Dysfunction (Pseudonormal): - E/A >1 (appears normal!) - DT 150–200 ms - LA pressure increases to "normalize" filling—requires Tissue Doppler to unmask. 4️⃣Grade III – Severe Dysfunction (Restrictive Pattern): - E/A >1.5 - DT <150 ms - Very high LA pressures, stiff LV—hallmark of poor prognosis. ⚠️Always correlate with tissue Doppler (E/e’), LA size, pulmonary vein flow, and clinical picture. A pseudonormal pattern can be misleading without thes...

Mortality Reducing Therapies in Chronic HFrEF: Evidence, Trials & Clinical Impact Heart failure with reduced ejection fraction (HFrEF) remains a major global cause of morbidity and mortality. Over the past three decades, rigorous randomized controlled trials (RCTs) have transformed management and proven that specific drugs and devices significantly reduce all-cause and cardiovascular mortality. Below is a comprehensive overview of each mortality-reducing therapy, its approximate relative mortality reduction, and the key landmark trials that shaped current guideline recommendations (AHA/ACC/HFSA & ESC). --- 1. Angiotensin Receptor Blockers (ARBs) — ~12% Mortality Reduction ARBs emerged as alternatives for patients intolerant to ACE inhibitors. They reduce afterload, neurohormonal activation, and remodeling. Landmark Trials • CHARM-Alternative (2003) Demonstrated mortality reduction in ACE-intolerant HFrEF patients with candesartan. • Val-HeFT (2001) Showed decreased HF hospitali...

  How to Differentiate Mitral Regurgitation (MR) vs Aortic Stenosis (AS) on CW Doppler and CW envelope SHAPE 1. Timing MR Holosystolic signal (throughout systole). Starts with isovolumic contraction and ends after A2 sometimes. No clear envelope edges. AS Mid-systolic envelope (starts after IVCT, ends before A2). Well-defined start and end. --- 2. Shape of CW Envelope Mitral Regurgitation (MR) Tall, dense, triangular (early-peaking) “V-shaped” or triangular because MR is often pressure-dependent. Peak velocity early then falls → early systolic peak (unless severe chronic MR → rounded). Aortic Stenosis (AS) Parabolic, rounded, symmetric envelope “Bullet shape” Peaks mid-systole (late peak if severe). --- 3. Velocity MR usually has higher velocity (5–6 m/s common). AS varies depending on severity but usually 3–5 m/s. --- 4. Direction & Position of CW Line MR CW is obtained from the apex directed posteriorly into the LA. AS CW is obtained in multiple windows (RUP parasternal, ap...

  A cup of coffee a day may cut AF recurrence — the DECAF trial (AHA late-breaking science) A surprising randomized trial presented as late-breaking science at the American Heart Association’s Scientific Sessions 2025 — and published in JAMA — found that patients with atrial fibrillation (AF) who were instructed to drink at least one cup of caffeinated coffee daily had fewer recurrences of AF or atrial flutter than those asked to abstain from all caffeine. The finding challenges long-standing advice that people with AF should avoid caffeinated beverages.  What the DECAF trial did DECAF (Does Eliminating Coffee Avoid Fibrillation?) was a randomized clinical trial that enrolled about 200 adults who had AF (or atrial flutter) and had recently undergone cardioversion. Participants were randomized 1:1 to (a) consume at least one cup of caffeinated coffee per day for six months or (b) completely abstain from coffee and other sources of caffeine for six months. The trial ran across m...