Dr. Usman's Cardiology Notes

 Athlete’s Heart vs Hypertrophic Cardiomyopathy (HCM) Distinguishing physiological cardiac adaptation from pathological hypertrophy is a high-yield clinical problem, especially in young athletes with increased LV wall thickness on echocardiography. The implications range from reassurance to sudden cardiac death prevention. --- Definitions Athlete’s Heart A benign, reversible structural and functional cardiac remodeling due to chronic intensive training (endurance or strength). It represents physiological hypertrophy. Hypertrophic Cardiomyopathy A genetic myocardial disease characterized by unexplained LV hypertrophy, myocyte disarray, and risk of arrhythmias and sudden cardiac death. --- Pathophysiology (Core Difference) Aspect Athlete’s Heart HCM Trigger Chronic training load Sarcomeric gene mutations Hypertrophy Adaptive Maladaptive Fibrosis Absent Present (interstitial/replacement) Reversibility Yes (deconditioning) No --- Echocardiographic Differences (Most Important) Feature A...

Tc-99m PYP Imaging for Cardiac Amyloidosis -- Introduction Cardiac amyloidosis is an under-recognized cause of heart failure with preserved ejection fraction, restrictive cardiomyopathy, and unexplained left ventricular hypertrophy. Tc-99m pyrophosphate (PYP) imaging has emerged as a pivotal, non-invasive test for diagnosing transthyretin cardiac amyloidosis (ATTR-CM) and has dramatically reduced the need for endomyocardial biopsy in appropriate clinical settings. --- What is Tc-99m PYP Imaging? Tc-99m PYP imaging is a nuclear scintigraphy technique that uses technetium-99m–labeled pyrophosphate, a bone-seeking tracer. In the heart, this tracer shows avid uptake in myocardium infiltrated by transthyretin amyloid, while uptake is minimal or absent in light-chain (AL) amyloidosis. --- Why is it Important? Provides non-invasive diagnosis of ATTR-CM Helps differentiate ATTR from AL amyloidosis Avoids unnecessary endomyocardial biopsy Enables early diagnosis and treatment, especially in HFp...

Brugada Algorithm for Wide-Complex Tachycardia VT vs SVT with Aberrancy Why the Brugada Algorithm Matters Wide-complex tachycardia (WCT) is ventricular tachycardia (VT) until proven otherwise. Mislabeling VT as supraventricular tachycardia (SVT) with aberrancy can lead to inappropriate therapy and hemodynamic collapse. The Brugada algorithm provides a stepwise, ECG-based approach to rapidly differentiate VT from SVT with aberrancy using standard 12-lead ECG features. --- When to Apply the Algorithm Regular WCT (QRS ≥ 120 ms) Stable or unstable patient (do not delay cardioversion in instability) No obvious pacing spikes or polymorphic rhythms --- Step-by-Step Brugada Algorithm --- Step 1: Absence of RS Complexes in All Precordial Leads (V1–V6) Look for RS complexes (an R wave followed by an S wave). If no RS complex in any precordial lead → VT Interpretation Pure monophasic R or S waves across V1–V6 strongly favor VT. --- Step 2: RS Interval > 100 ms in Any Precordial Lead Measure fr...

  Criteria of Culprit Artery in Inferior Wall STEMI Identifying the culprit artery (RCA vs LCX) in inferior wall STEMI from surface ECG helps anticipate complications, guide cath strategy, and assess myocardial area at risk. This post summarizes ECG-based criteria commonly used to differentiate RCA from LCX occlusion. ST Elevation in Leads III and II Key principle: Lead III reflects RCA territory more strongly than lead II Findings favoring RCA occlusion ST elevation in lead III > lead II ST depression in aVL greater than lead I These patterns indicate an injury vector directed inferiorly and rightward, consistent with RCA involvement. --- Role of Lateral Precordial Leads (V5–V6) --- V5 and V6 have limited value in differentiating RCA from LCX occlusion Presence of ST elevation in V5–V6 suggests: Larger myocardial area at risk Possible extension beyond isolated inferior infarction They should be interpreted as markers of infarct size rather than culprit artery. --- ST-Segment Be...

Arterial Pulse Waveforms – Clinical Interpretation and Significance --- Importance of Pulse Waveform Analysis Examination of the arterial pulse is a powerful bedside tool. Beyond rate and rhythm, the contour, amplitude, and timing of the pulse provide clues to underlying valvular disease, cardiomyopathy, and ventricular function. Pulse waveform abnormalities often mirror left ventricular systolic dynamics and arterial compliance. --- Normal Pulse A normal arterial pulse has: Rapid upstroke Smooth systolic peak Gradual downstroke It reflects normal left ventricular ejection, intact aortic valve function, and compliant arterial system. --- Water Hammer Pulse (Collapsing Pulse) Key Features Bounding, forceful pulse Rapid upstroke followed by sudden collapse Wide pulse pressure Mechanism High systolic pressure from increased stroke volume combined with rapid diastolic runoff leads to abrupt arterial collapse. Common Associations Aortic regurgitation High-output states (e.g., anemia, thyrot...

  Diagnostic Algorithm for Narrow Complex Tachycardia (NCT) Narrow complex tachycardia refers to a regular or irregular tachyarrhythmia with QRS duration <120 ms, implying ventricular activation via the normal His–Purkinje system. A systematic ECG-based approach allows rapid and accurate diagnosis at the bedside. Step 1: Confirm It Is a Narrow Complex Tachycardia QRS duration <120 ms Ventricular rate usually >100 bpm If QRS is borderline, consider aberrancy or pre-excited tachycardia separately Step 2: Assess Regularity of RR Interval A. Regular Narrow Complex Tachycardia Common causes: AVNRT AVRT (orthodromic) Atrial tachycardia Atrial flutter with fixed AV conduction (usually 2:1) B. Irregular Narrow Complex Tachycardia Common causes: Atrial fibrillation Atrial flutter with variable AV block Multifocal atrial tachycardia Step 3: Look for P Waves and Their Relationship to QRS Are P waves visible? Clearly visible before QRS → likely atrial ta...

  COMPANION Trial (Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure) Heart failure with reduced ejection fraction (HFrEF) remains a major cause of morbidity and mortality despite advances in pharmacological therapy. Electrical dyssynchrony, reflected by a wide QRS complex, contributes significantly to progressive ventricular dysfunction. The COMPANION trial was a landmark study that established the role of cardiac resynchronization therapy (CRT), with or without a defibrillator, in patients with advanced heart failure. --- Background and Rationale Prior to COMPANION, optimal medical therapy (OMT) was the cornerstone of heart failure management. However, many patients with severe systolic dysfunction and prolonged QRS continued to experience recurrent hospitalizations and high mortality. CRT was developed to correct interventricular and intraventricular dyssynchrony by simultaneous pacing of both ventricles. COMPANION was designed to determine whether addin...