No abstract

Doppler echocardiography was performed in 136 patients with a normally functioning prosthetic valve in the aortic (n = 59), mitral (n = 74) and tricuspid (n = 3) positions. These included patients with St. Jude (n = 82), Björk-Shiley (n = 18), Beall (n = 13), Starr-Edwards (n = 7) or tissue (n = 16) valves. Peak and mean pressure gradients across the prostheses were measured using the simplified Bernoulli equation. The prosthetic valve orifice (PVO, in square centimeters), only in the mitral position, was calculated by the equation: PVO = 220/pressure half-time. In the aortic position, the St. Jude valve had a lower peak velocity (2.3 +/- 0.6 m/s, range 1.0 to 3.9), peak gradient (22 +/- 12 mm Hg, range 4 to 61) and mean gradient (12 +/- 7 mm Hg, range 2 to 32) than the other valves (p less than 0.05) when compared with Starr-Edwards). In the mitral position, the St. Jude valve had the largest orifice (3.0 +/- 0.6 cm2, range 1.8 to 5.0) (p less than 0.0001 compared with all other valves). Insignificant regurgitation was commonly found by pulsed mode Doppler technique in patients with a St. Jude or Björk-Shiley valve in the aortic or mitral position and in patients with a Starr-Edwards or tissue valve in the aortic position. In 17 other patients with a malfunctioning prosthesis (four St. Jude, two Björk-Shiley, four Beall and seven tissue valves) proven by cardiac catheterization, surgery or autopsy, Doppler echocardiography correctly identified the complication (significant regurgitation or obstruction) in all but 2 patients who had a Beall valve. It is concluded that 1) the St. Jude valve appears to have the most optimal hemodynamics; mild regurgitation can be detected by the Doppler technique in normally functioning St. Jude and Björk-Shiley valves in the aortic or mitral position and in Starr-Edwards and tissue valves in the aortic position, and 2) Doppler echocardiography is a useful method for the detection of prosthetic valve malfunction, especially when the St. Jude, Björk-Shiley and tissue valves are assessed.

M-mode and Doppler echocardiography were performed in 16 patients with first degree atrioventricular (AV) block, 1 patient with second degree (Wenckebach type) and 3 patients with third degree AV block; 20 individuals with a normal PR interval served as control subjects. The time from the onset of the P wave to the mitral valve closure by M-mode and to the end of mitral flow by Doppler echocardiography were obtained. In 20 normal subjects, the P wave to mitral valve closure interval measured 220 +/- 30 ms by M-mode and to the end of mitral flow 225 +/- 29 ms by Doppler technique (p = NS). In patients with first degree AV block, these intervals measured 242 +/- 41 and 249 +/- 36 ms, respectively (p = NS). Late diastolic (before the onset of the QRS complex) mitral regurgitation was detected by pulsed mode Doppler imaging in 9 (56%) of the 16 patients with first degree AV block but in none with a normal PR interval. In the four patients with advanced AV block, intermittent mid or late diastolic mitral regurgitation was found to depend on the position of the P wave in diastole. With early diastolic P waves, the end of mitral valve flow by Doppler technique occurred 230 to 250 ms after the onset of the P wave and was followed by mild diastolic mitral regurgitation of variable duration. With P waves falling in systole, the mitral valve remained open throughout diastole; during most of diastole, however, there was neither forward mitral flow (diastasis) nor diastolic mitral regurgitation detected by Doppler technique.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular hypertrophy is an important adaptive response to chronic pressure or volume overload of the left ventricle. The different types and the pathophysiologic mechanisms of the development of left ventricular hypertrophy in various disease states are reviewed. Detection of left ventricular hypertrophy may be accomplished by electrocardiography and cardiac angiography. Echocardiography, however, is the most accurate noninvasive method to detect the presence and estimate the severity of increased left ventricular mass. The clinical significance of left ventricular hypertrophy and its prognostic implications in several cardiac diseases associated with hypertrophy are discussed. The critical transition stage from adaptive, compensatory and reversible left ventricular hypertrophy to "pathologic" hypertrophy with impaired left ventricular contractility and irreversible myocardial damage is yet unknown. Recent data are presented that provide evidence of regression of left ventricular hypertrophy after medical treatment of patients with hypertension and after aortic valve replacement in patients with aortic valve disease. The clinical importance of regression of hypertrophy and its effects on long-term prognosis remain to be determined.

To determine the cardiac rhythm disturbances underlying sudden death, 15 patients (14 inpatients and 1 outpatient) who had cardiac arrest unexpectedly while undergoing ambulatory electrocardiographic monitoring were identified. Heart disease was present in 11 patients and 7 patients were admitted to the hospital with chest pain before sudden cardiac death occurred. The terminal event at the time of cardiac arrest in 3 (20%) of the 15 patients was a bradyarrhythmia expressed as complete heart block; none survived. A ventricular tachyarrhythmia was the precursor of sudden cardiac death in the remaining 12 patients (80%). Two of these 12 had slow ventricular tachycardia and both died. Five had polymorphous ventricular tachycardia associated with prolonged QT interval (torsade de pointes) and three were receiving a class I antiarrhythmic agent. This rhythm degenerated into ventricular fibrillation in one patient; four of the five patients survived after electrical cardioversion. One patient had ventricular tachycardia followed by asystole. Four patients had ventricular flutter (rate greater than 250/min) that degenerated into ventricular fibrillation in each case; only one of these four patients survived after cardioversion. Frequent (greater than 30/h) premature ventricular complexes were present in 9 of 10 patients with ventricular tachycardia or flutter and R on T phenomenon was seen in only 1 patient. In conclusion, a ventricular tachyarrhythmia is usually found on Holter monitoring during sudden cardiac death in hospitalized patients; torsade de pointes (polymorphous ventricular tachycardia) is a frequent cause of sudden death in these patients. Ventricular fibrillation is always preceded by ventricular tachycardia or ventricular flutter.