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Left ventricular hypertrophy with secondary repolarization abnormalities as seen on ECG Histopathology of (a) normal myocardium and (b) myocardial hypertrophy. Scale bar indicates 50 μm. Gross pathology of left ventricular hypertrophy. Left ventricle is at right in image, serially sectioned from apex to near base.
The diagnosis of left ventricular outflow tract obstruction is usually made by echocardiographic assessment and is defined as a peak left ventricular outflow tract gradient of ≥ 30 mmHg. [ 35 ] Another, non-obstructive variant of HCM is apical hypertrophic cardiomyopathy ( AHCM or ApHCM ), [ 37 ] also called Yamaguchi syndrome .
In electrocardiography, a strain pattern is a well-recognized marker for the presence of anatomic left ventricular hypertrophy (LVH) in the form of ST depression and T wave inversion on a resting ECG. [1] It is an abnormality of repolarization and it has been associated with an adverse prognosis in a variety heart disease patients.
Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart. [ 1 ] [ better source needed ] Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur.
Left anterior fascicular block (LAFB) is an abnormal condition of the left ventricle of the heart, [1] [2] related to, but distinguished from, left bundle branch block (LBBB). It is caused by only the left anterior fascicle – one half of the left bundle branch being defective. It is manifested on the ECG by left axis deviation.
This delays the onset of the intrinsicoid deflection. This prolongation or delay is an important criterion for diagnosing bundle branch block or ventricular hypertrophy. Time of onset of intrinsicoid deflection > 0.04 seconds (just over one small box) is used as a non-voltage related criterion to diagnose left ventricular hypertrophy. [2]
The clinician must therefore be well versed in recognizing the so-called ECG mimics of acute myocardial infarction, which include left ventricular hypertrophy, left bundle branch block, paced rhythm, early repolarization, pericarditis, hyperkalemia, and ventricular aneurysm. [7] [8] [9] Localisation of the occlusion in the ECG showing STEMI changes
Horizontal ST depression in V4, V5, V6 leads during a cardiac stress ECG. Other, non-ischemic, causes include: Side effect of digoxin [4] [3] Hypokalemia [4] [3] Right or left ventricular hypertrophy [3] Intraventricular conduction abnormalities (e.g., right or left bundle branch block, WPW, etc.) [3] Hypothermia [4] Tachycardia [4] Reciprocal ...