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Showing posts from December, 2025

Brugada ECG Patterns

  Brugada ECG Patterns: A Comprehensive, Clinically Oriented Guide Overview Brugada syndrome is an inherited cardiac ion-channel disorder characterized by distinctive ECG patterns in the right precordial leads and an increased risk of malignant ventricular arrhythmias and sudden cardiac death (SCD), often in structurally normal hearts. The ECG phenotype is dynamic and may be concealed, unmasked, or modulated by fever, drugs, and autonomic tone. --- ECG Patterns of Brugada Syndrome Type 1 (Diagnostic Pattern) Key features Coved ST-segment elevation ≥2 mm in ≥1 right precordial lead (V1–V3) Followed by a negative T wave J-point elevation with downsloping ST segment Clinical significance Only ECG pattern diagnostic of Brugada syndrome (when present spontaneously or induced by sodium-channel blocker) High arrhythmic risk, especially if spontaneous and associated with symptoms --- Type 2 (Suggestive Pattern) Key features Saddleback ST elevation ≥2 mm ST segment remains elevated ≥1 mm Po...

Factors Affecting BNP Levels

  Factors Affecting BNP Levels B-type natriuretic peptide (BNP) is released predominantly from ventricular myocardium in response to increased wall stress. Although widely used for diagnosis, prognosis, and treatment guidance in heart failure, BNP levels are influenced by multiple cardiac and non-cardiac factors. Understanding these modifiers is essential to avoid misinterpretation. Physiological and Demographic Factors Age BNP levels rise progressively with age, even in the absence of heart failure. Elderly patients may have “false-positive” elevations. Sex Women have higher baseline BNP levels than men, likely related to hormonal influences and myocardial gene expression. Body Mass Index Obesity is associated with lower BNP levels due to increased clearance by adipose tissue and reduced myocardial secretion. Normal BNP does not exclude heart failure in obese patients. Genetic Variability Inter-individual genetic differences affect natriuretic peptide synthesis, secretion, and deg...

Propafenone “organizes” atrial fibrillation

PROPAFENONE — KEY POINTS (Class IC Antiarrhythmic) Mechanism Potent fast Na⁺ channel blocker Marked slowing of atrial & ventricular conduction Use-dependent effect (stronger at higher heart rates) Mild β-blocking activity Effect on Atrial Fibrillation Reduces multiple chaotic atrial wavelets Organizes AF → atrial flutter / atrial tachycardia Facilitates pharmacologic or electrical cardioversion ECG Effects ↑ PR interval ↑ QRS duration (rate-dependent) Little effect on QT (no significant AP prolongation) Aberrancy / Wide QRS Due to use-dependent Na⁺ channel block Causes functional bundle branch block at high rates QRS widens during tachycardia, narrows when rate slows Clinical Use Rhythm control in AF / SVT “Pill-in-the-pocket” strategy (selected patients) Important Precautions ❌ Avoid in structural heart disease ❌ Avoid in ischemic heart disease / LV dysfunction Always combine with AV-nodal blocker (β-blocker or diltiazem/verapamil) One-Line Memory Propafenone slows conduction, org...

Pericardial Fat Pad Mimicking Cardiomegaly

 Pericardial Fat Pad Mimicking Cardiomegaly: Cause of Increased Cardiothoracic Ratio on Chest X-Ray Introduction An increased cardiothoracic ratio (CTR) on chest X-ray (CXR) is commonly interpreted as cardiomegaly. However, not all apparent cardiac enlargement reflects true cardiac pathology. One important and often overlooked cause is a pericardial fat pad, which can enlarge the cardiac silhouette without any increase in actual heart size. Recognizing this entity is essential to avoid misdiagnosis and unnecessary investigations. --- What Is a Pericardial Fat Pad? Pericardial fat refers to adipose tissue located: Epicardial fat: between the myocardium and visceral pericardium Paracardial (mediastinal) fat: outside the parietal pericardium When excessive, this fat can project over the cardiac borders on CXR, producing a falsely increased CTR. --- Why It Increases CTR on Chest X-Ray CTR is calculated as the ratio of maximal transverse cardiac diameter to maximal thoracic diameter (no...

ESC Guidelines: Adenosine Response in Regular Narrow Complex Tachycardia (NCT)

Adenosine Response in Regular Narrow Complex Tachycardia (NCT) 🫀⚡ Regular narrow complex tachycardia (QRS < 120 ms) is most commonly due to supraventricular tachycardias (SVTs). Adenosine is both a diagnostic and therapeutic agent in this setting because of its transient AV nodal block. Understanding the ECG response to adenosine is crucial for accurate rhythm diagnosis at the bedside, emergency department, and EP lab. --- Mechanism of Action of Adenosine Adenosine acts primarily on A1 receptors in the AV node, leading to: Hyperpolarization of AV nodal tissue Transient complete AV block Very short half-life (≈ 10 seconds) This makes adenosine ideal for unmasking atrial activity or terminating AV node–dependent tachycardias. --- Why Adenosine Is Useful in Regular NCT In regular NCT, the differential diagnosis includes: AV nodal–dependent tachycardias Atrial tachyarrhythmias with rapid ventricular response Adenosine helps by answering one key question: Is the AV node essential for ma...

Average LDL-C reduction with lipid-lowering therapies (ESC/EAS)

  Average LDL-C reduction with lipid-lowering therapies (ESC/EAS): ■ Statins are the foundation: Moderate-intensity ≈ 30% High-intensity ≈ 50% ■ Statin + non-statin combinations markedly improve efficacy: High-intensity statin + ezetimibe ≈ 60% High-intensity statin + bempedoic acid ≈ 58% ■ PCSK9 inhibitors provide the largest incremental effect: PCSK9 mAb alone ≈ 60% With statins ± ezetimibe → 75–80% ■ Maximal LDL-C lowering (~85–86%) is achieved with quadruple therapy (high-intensity statin + ezetimibe + bempedoic acid + PCSK9 mAb). ■ Clinical implication: very-high-risk patients usually require early combination therapy to reach ESC LDL-C targets. #medical #cardiology #hearthealth #heart #fblifestyle

Bedside Hemodynamic Assessment: An Echocardiography Guide for the ICU

  Bedside Hemodynamic Assessment: An Echocardiography Guide for the ICU Bedside echocardiography has become a cornerstone of modern ICU practice. Beyond simple assessment of left ventricular ejection fraction, focused echocardiography allows real-time evaluation of pressures, congestion, systemic flow, and shock physiology. A structured approach transforms echo from a descriptive tool into a true hemodynamic monitor. --- 1. Role of Echocardiography in ICU Hemodynamics Critically ill patients often have complex, rapidly changing physiology. Invasive monitoring is not always available or reliable. Bedside echocardiography provides: • Non-invasive, repeatable hemodynamic assessment • Immediate correlation with clinical status • Guidance for fluids, inotropes, and vasopressors • Etiologic diagnosis of shock A practical framework divides assessment into two domains: 1. Pressures and congestion 2. Systemic flow and shock state --- 2. Assessing Pressures and Venous Congestion A. Inferior ...

Systolic Anterior Motion (SAM) in Hypertrophic Cardiomyopathy

Systolic Anterior Motion (SAM) in Hypertrophic Cardiomyopathy Definition Systolic anterior motion (SAM) refers to anterior displacement of the mitral valve apparatus toward the interventricular septum during systole, leading to dynamic left ventricular outflow tract (LVOT) obstruction and mitral regurgitation. It is a hallmark pathophysiologic feature of hypertrophic cardiomyopathy (HCM), particularly the obstructive phenotype. --- Pathophysiology of SAM SAM is not simply a consequence of septal hypertrophy; it is the result of complex interactions between ventricular geometry, mitral valve anatomy, and flow dynamics. Key mechanisms include: 1. Venturi and Drag Forces High-velocity systolic flow through a narrowed LVOT creates drag forces that pull the anterior mitral leaflet toward the septum. 2. Mitral Valve Abnormalities Elongated anterior mitral leaflet Anterior displacement of papillary muscles Increased leaflet slack These abnormalities predispose the leaflet to systolic displace...

Evolution of ECG Changes in STEMI

Evolution of ECG Changes in STEMI ST-elevation myocardial infarction (STEMI) produces a characteristic, time-dependent sequence of ECG changes that reflect ongoing myocardial ischemia, injury, and eventual necrosis. Understanding this evolution is critical for early diagnosis, localization of the infarct-related artery, reperfusion decisions, and assessment of infarct age. --- 1. Hyperacute Phase (Minutes to First Hour) Key ECG features Tall, broad-based, symmetrical T waves T wave height disproportionate to QRS complex Often localized to a coronary territory ST segment may still be isoelectric or minimally elevated Pathophysiology Local extracellular potassium accumulation due to acute transmural ischemia Earliest electrical manifestation of coronary occlusion Clinical relevance Easily missed or mistaken for hyperkalemia Recognition allows ultra-early reperfusion before ST elevation becomes obvious --- 2. Acute Injury Phase (Minutes to Hours) Key ECG features ST-segment elevation in c...

Broken Heart Syndrome (Takotsubo Syndrome, Stress Cardiomyopathy)

 Broken Heart Syndrome (Takotsubo Syndrome, Stress Cardiomyopathy) Definition Broken heart syndrome, also known as Takotsubo syndrome (TTS), is an acute, reversible heart failure syndrome characterized by transient left ventricular systolic dysfunction, usually triggered by intense emotional or physical stress, in the absence of obstructive coronary artery disease sufficient to explain the presentation. Epidemiology Predominantly affects postmenopausal women (≈85–90%) Accounts for 1–3% of patients presenting with suspected acute coronary syndrome (ACS) Increasing recognition due to routine coronary angiography and cardiac MRI Pathophysiology (Guideline-based concepts) Exact mechanism remains multifactorial and incompletely understood. Current ESC and international consensus emphasize: Catecholamine excess Sudden surge in catecholamines leading to myocardial stunning, microvascular dysfunction, and direct myocyte toxicity Coronary microvascular dysfunction Impaired coronary flow res...

MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries)

MINOCA (Myocardial Infarction with Non-Obstructive Coronary Arteries) Definition: MINOCA is defined as an acute myocardial infarction fulfilling the universal MI criteria, with coronary angiography showing no obstructive coronary artery disease (no stenosis ≥50%) and no alternative non-ischemic explanation at the time of angiography. It is a working diagnosis rather than a final one. Epidemiology • Accounts for ~5–10% of all myocardial infarctions • More common in women and younger patients • Prognosis is not benign and carries a significant risk of recurrent events and mortality Diagnostic Criteria (ESC-based) According to the European Society of Cardiology, all of the following must be present: 1. Clinical evidence of acute myocardial infarction – Ischemic symptoms – ECG changes consistent with MI – Rise and/or fall of cardiac troponin 2. Non-obstructive coronary arteries on angiography (<50% stenosis) 3. No overt alternative diagnosis at presentation (e.g. sepsis, pulmonary embol...

Diastolic dysfunction on echocardiography

Diastolic dysfunction on echocardiography: a comprehensive, guideline-oriented review Diastolic dysfunction refers to impaired left ventricular (LV) filling due to abnormal relaxation, increased chamber stiffness, or both, leading to elevated LV filling pressures. It is a central mechanism in heart failure with preserved ejection fraction (HFpEF) and contributes significantly to symptoms, prognosis, and management decisions. PHYSIOLOGY OF DIASTOLE LV diastole has four phases: 1. Isovolumic relaxation (IVRT): energy-dependent myocardial relaxation after aortic valve closure 2. Early rapid filling: pressure gradient–driven filling (E wave) 3. Diastasis: minimal flow when LA and LV pressures equalize 4. Atrial contraction: late filling (A wave) Diastolic dysfunction develops when relaxation is delayed, compliance is reduced, or left atrial (LA) pressure rises to compensate. ECHOCARDIOGRAPHIC PARAMETERS FOR DIASTOLIC ASSESSMENT 1. Mitral inflow Doppler Measured in apical 4-chamber view wit...

Localizing MI on ECG

  Localizing Myocardial Infarction (MI) on ECG A Practical, Clinically Oriented Guide --- Why ECG Localization Matters Accurate localization of MI on ECG helps to: Identify the culprit coronary artery Predict complications (heart block, papillary muscle rupture, RV infarction) Guide urgent reperfusion strategy Correlate with echocardiography and angiography findings --- Basic ECG Principles in MI Localization ST-segment elevation reflects acute transmural injury ST-segment depression may represent reciprocal change or subendocardial ischemia T-wave inversion indicates evolving or prior ischemia Pathological Q waves suggest established infarction Key rule: Always interpret ECG in clinical context and with serial tracings. --- ECG Leads and Myocardial Territories Inferior Wall MI Leads: II, III, aVF Common artery: Right coronary artery (RCA) Key points: ST elevation often greater in III than II → favors RCA Check for associated RV infarction Reciprocal ST depression in I and aVL Comp...

Heart failure with preserved ejection fraction (HFpEF)

Heart failure with preserved ejection fraction (HFpEF): diagnosis and management A comprehensive, guideline-oriented clinical review --- Definition and epidemiology Heart failure with preserved ejection fraction (HFpEF) is defined as clinical heart failure with a left ventricular ejection fraction (LVEF) ≥50%, evidence of cardiac structural and/or functional abnormalities, and elevated filling pressures at rest or during stress. HFpEF accounts for ~50% of all heart failure cases and its prevalence continues to rise due to population aging and increasing burden of hypertension, obesity, diabetes, and chronic kidney disease. Mortality remains comparable to HFrEF, with frequent hospitalizations and poor quality of life. --- Pathophysiology: why HFpEF is complex HFpEF is not a single disease but a syndrome driven by systemic inflammation and multiorgan dysfunction. Key mechanisms include: • Left ventricular diastolic dysfunction (impaired relaxation + increased stiffness) • Concentric remo...

Tenecteplase Dosing

 Tenecteplase: expanding horizons in thrombolytic therapy across various clinical indications Tenecteplase: Expanding Horizons in Thrombolytic Therapy Across Clinical Indications Tenecteplase is a genetically engineered variant of tissue plasminogen activator (tPA) developed to improve fibrinolytic efficacy, ease of administration, and safety compared with alteplase. Its pharmacological advantages have driven growing interest beyond its original indication in ST-elevation myocardial infarction (STEMI), with expanding roles in acute ischemic stroke and other thrombotic conditions. What Is Tenecteplase Tenecteplase is a fibrin-specific thrombolytic agent produced by recombinant DNA technology. It differs from alteplase by three amino acid substitutions, resulting in enhanced fibrin specificity and resistance to plasminogen activator inhibitor-1 (PAI-1). Key Pharmacological Advantages • Single IV bolus administration (no infusion) • Longer plasma half-life • Greater fibrin specificity...

Compaction ratio for diagnosis of LVNC

Compaction ratio for diagnosis of LVNC. Epicardium- to- trabecular- trough thickness is termed compacted myocardium (C), and trabecular- peak- to- trough thickness is termed non- compacted myocardium (NC). LVNC is considered when NC/ C is greater than 2 by echocardiography and 2.3 by magnetic resonance imaging. Compaction Ratio for Diagnosis of Left Ventricular Non-Compaction (LVNC) Overview Left Ventricular Non-Compaction (LVNC) cardiomyopathy is a structural myocardial disorder characterized by a two-layered left ventricular (LV) wall consisting of a thin, compacted (C) epicardial layer and an abnormally thickened non-compacted (NC) trabecular layer with deep recesses communicating with the LV cavity. LVNC is considered a genetic or primary cardiomyopathy, though increased trabeculation alone may also be seen in healthy individuals, athletes, or pregnancy, making accurate diagnosis essential.  Compaction Ratio Criteria The main imaging modalities used to assess LVNC are transthor...