Dr. Usman's Cardiology Notes

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: 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 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): 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: 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. 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...

Bartter, Liddle, and Conn Syndromes A practical comparison of salt-handling disorders causing metabolic alkalosis Disorders of renal sodium handling are frequently tested and clinically relevant because they present with characteristic patterns of blood pressure, electrolytes, and hormonal changes. Bartter syndrome, Liddle syndrome, and Conn syndrome all cause metabolic alkalosis but differ fundamentally in their mechanisms and clinical profiles. --- Bartter Syndrome Salt-wasting disorder mimicking chronic loop diuretic use Bartter syndrome is a hereditary defect of ion transport in the thick ascending limb of the loop of Henle, most commonly involving the Na–K–2Cl cotransporter (NKCC2) or related channels. Pathophysiology Impaired sodium reabsorption in the loop of Henle Renal sodium loss → extracellular volume depletion Secondary activation of RAAS Increased distal sodium delivery → potassium and hydrogen ion loss Key Biochemical Changes Increased Renin Aldosterone Decreased Sodium B...