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ECG and Left Ventricular Aneurysm

ECG and Left Ventricular Aneurysm Left ventricular (LV) aneurysm is a late mechanical complication of transmural myocardial infarction, most commonly following an anterior wall STEMI. Recognizing its characteristic ECG pattern is crucial because it can closely mimic acute STEMI and may lead to unnecessary thrombolysis or cath lab activation if misinterpreted. What Is a Left Ventricular Aneurysm A left ventricular aneurysm is a thin, scarred, dyskinetic segment of myocardium that bulges outward during systole. It usually develops weeks after a full-thickness myocardial infarction due to replacement of necrotic myocardium with fibrous tissue. ECG Changes in Left Ventricular Aneurysm The ECG findings are distinctive and relatively stable over time. Distribution of ECG Changes ECG abnormalities are most commonly seen in the precordial leads, especially V1 to V6, reflecting involvement of the anterior wall. Inferior lead involvement (II, III, aVF) is uncommon unless the aneurysm involves th...

Indications of left atrial appendage (LAA) device closure

Indications of left atrial appendage (LAA) device closure: Patients with non-valvular atrial fibrillation who have an increased risk of stroke (CHA₂DS₂-VASc score ≥2 in men or ≥3 in women) and are not suitable for long-term oral anticoagulation. Absolute contraindication to long-term oral anticoagulants: History of major or life-threatening bleeding (e.g., intracranial hemorrhage). Active bleeding disorder or high-risk bleeding lesion. Severe thrombocytopenia or advanced liver disease with coagulopathy. Relative contraindication or intolerance to oral anticoagulation: Recurrent clinically significant bleeding while on adequate anticoagulation. Poor tolerance or allergy to anticoagulants. Inability to maintain stable INR on warfarin. Poor adherence or inability to take long-term anticoagulant therapy. High bleeding risk despite indication for anticoagulation: HAS-BLED score ≥3 with anticipated long-term bleeding risk. Elderly patients with frequent falls or frailty where bleeding risk o...

Dilated Pulmonary Artery in Marfan syndrome

Dilated Pulmonary Artery in Marfan syndrome Overview Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the FBN1 gene, leading to abnormal fibrillin-1 and weakness of elastic tissues. Cardiovascular involvement classically affects the aorta, but dilation of the pulmonary artery (PA) is a recognized, though under-discussed, manifestation. Pulmonary artery dilation in Marfan syndrome reflects the same underlying medial degeneration that affects the aorta and can have diagnostic and prognostic significance. Pathophysiology The pulmonary artery wall, like the aorta, is rich in elastic fibers. In Marfan syndrome, defective fibrillin-1 results in: • Fragmentation of elastic fibers • Medial degeneration and cystic medial necrosis • Reduced tensile strength of the vessel wall Although pulmonary artery pressures are normally much lower than systemic pressures, chronic exposure to abnormal wall stress can still lead to progressive dilation. This explains w...

Hemodynamic Formulas to remember

  Hemodynamic formulas are fundamental tools in cardiology and critical care, allowing clinicians to quantify cardiac performance, vascular tone, and circulatory efficiency. Understanding these calculations helps in diagnosing shock states, guiding fluid therapy, titrating vasoactive drugs, and interpreting invasive hemodynamic monitoring. Cardiac Output (CO) and Cardiac Index (CI): Cardiac output represents the volume of blood pumped by the heart per minute and is calculated as stroke volume multiplied by heart rate (CO = SV × HR). Normal CO ranges from 4–8 L/min. Because CO varies with body size, cardiac index adjusts CO for body surface area (CI = CO/BSA), providing a more accurate assessment of cardiac performance. A normal CI is 2.2–4.0 L/min/m². Low CI suggests pump failure or hypovolemia, while high CI is seen in sepsis or hyperdynamic states. Stroke Volume (SV) and Stroke Volume Index (SVI): Stroke volume is the amount of blood ejected from the left ventricle with each hear...

Acute Pericarditis

Acute Pericarditis – A Complete Clinical Guide for Practice Definition Acute pericarditis is an inflammatory condition of the pericardium lasting less than 4–6 weeks. It is a common cause of acute chest pain and should always be differentiated from acute coronary syndromes. Epidemiology Acute pericarditis accounts for approximately 5% of emergency department visits for chest pain not related to myocardial infarction. It affects all age groups, with a slight male predominance. Etiology In most cases, acute pericarditis is idiopathic, presumed viral. Common causes include: • Viral: Coxsackievirus, echovirus, influenza, COVID-19 • Bacterial: Tuberculosis (important in endemic regions), staphylococci, streptococci • Post–myocardial injury: Early post-MI, Dressler syndrome • Autoimmune: SLE, rheumatoid arthritis • Metabolic: Uremia • Neoplastic: Lung, breast, lymphoma • Drug-induced and radiation-related Clinical Presentation Chest Pain • Sharp, pleuritic chest pain • Worse on inspiration a...

True vs pseudo mitral annular dysjunction on echocardiography

True mitral annular disjunction (MAD) is a genuine structural abnormality in which there is a real separation between the hinge point of the posterior mitral leaflet and the left ventricular myocardium. On echocardiography, especially in parasternal long-axis view during systole, the mitral annulus is seen displaced atrially with a clear gap between the annulus and the ventricular wall. This separation persists consistently, is best appreciated in systole, and is often associated with mitral valve prolapse, excessive annular motion, and sometimes ventricular arrhythmias. Pseudo mitral annular disjunction is an apparent or false impression of annular separation caused by imaging artifacts or altered cardiac geometry rather than a true anatomic defect. It may be seen due to oblique imaging planes, heavy mitral annular calcification, leaflet billowing, translational motion of the heart, or marked left atrial enlargement. In pseudo MAD, the apparent gap disappears with correct probe alignm...

Early Repolarization: Classic vs New Definitions

Early Repolarization: Classic vs New Definitions Explained Early repolarization (ER) is a common ECG finding, long considered benign, but modern understanding has refined its definition and clinical relevance. This article explains the classic and newer definitions of early repolarization using ECG morphology, focusing on the J-point, J-wave, ST segment, and terminal QRS changes. Introduction Early repolarization refers to ECG patterns reflecting changes at the end of ventricular depolarization and the beginning of repolarization. Traditionally associated with ST elevation in young, healthy individuals, ER is now defined more precisely based on J-point morphology rather than ST elevation alone. Classic Definition of Early Repolarization The classic definition of early repolarization was centered on ST-segment elevation. Key ECG Features (Classic Definition) 1. J-point elevation The J-point is elevated above the baseline, typically ≥1 mm. 2. Concave upward ST elevation The ST segment sh...