Phonocardiographic findings in patients with normally functioning Ionescu-Shiley prostheses.

Phonocardiographic findings are reported in 19 patients with normally functioning Ionescu-Shiley prostheses in the mitral or aortic position. Opening clicks were recorded in all 8 patients with mitral prostheses at a mean second heart sound (A2) to opening click interval of 94 ms. In 9 subjects, apical systolic murmurs were found. All 11 patients with the prosthesis in the aortic position had systolic ejection murmurs. Opening clicks were observed in 8 patients with a mean Q wave to opening click interval of 125 ms; closing clicks were found in 9 of 11. No diastolic murmurs occurred in this group. These acoustic characteristics serve as a reference source for the noninvasive evaluation of the bovine pericardial prosthesis.

"Push-up palpitations": unusual presentation of ruptured chordae tendineae: a case report.

A 47-year-old man experienced palpitations and shortness of breath following push-up exercises. Because of paroxysmal atrial fibrillation and fatigue, the patient underwent investigation. Echocardiography and cardiac catheterization indicated the diagnoses of mitral valve prolapse and rupture of the chordae tendineae. This report represents the first description of such a sequence of events.

Septal aneurysm and right ventricular obstruction: a case report.

A 32-year-old man with a history of ventricular septal defect presented with systolic and diastolic murmurs and vectocardiographic evidence of right ventricular hypertrophy. Echocardiography demonstrated a prominent systolic bulging of the interventricular septum into the right ventricle. Left ventricular angiograms indicated that the ultrasonic abnormality was based on an aneurysm of the membranous septum which produced a 35 mm Hg gradient within the right ventricle. After plication of this aneurysm, murmur and abnormal septal protrusion were not recorded.

Hypertrophy or dilatation? A vectorial analysis of echocardiographically determined left ventricular enlargement.

Echocardiograms (ECHO) and Frank vectorcardiograms (VCGs) were obtained in three groups of patients: Group I (n = 16), concentric left ventricular hypertrophy (LVH) with increased interventricular septal (IVS) and left ventricular posterior wall (LVPW) thickness in the presence of a normal left ventricular internal dimension (LVID); Group II (n = 17), left ventricular dilatation (LVD) with an enlarged LVID, normal IVS and LVPW thickness, and Group III (n = 22), no catheterization evidence of heart disease with normal IVS, LVPW and LVID. VCGs were analyzed with respect to magnitude of the QRS maximal deflection vector (MDV) and +/- 10 msec QRS vectors, horizontal plane (HP) maximal posterior force, time of HP MDV inscription, distal and proximal HP loop areas and HP loop configuration utlizing criteria of Varriale et al. The results indicate that: 1) HP QRS vector magnitude cannot reliably differentiate concentric LVH from isolated LVD and 2) proximal-distal loop area relationships and pattern of the HP QRS loop, when reviewed together, are superior to other criteria for distinguishing whether ECHO determined LVH or LVD is the primary correlate of an enlarged left ventricle.

Eelectrocardiographic correlates of ultrasonically increased septal, left ventricular posterior wall and left ventricular internal dimensions.

The electrocardiograms (ECG) of 64 subjects who exhibited an echocardiographically demonstrable increase in thickness of the interventricular septum and left ventricular posterior wall (Group 1, 22 patients), isolated left ventricular internal dimension (Group 2,26 patients), combined wall thickness and chamber diameter (Group 3, 2 patients), and septal thickness, (Group 4, asymmetric septal hypertrophy, 14 patients) were reviewed in order to determine sensitivity of ECG criteria for the diagnosis of left ventricular hypertrophy (LVH) proposed in 1949 by Sokolow and Lyon (13), in 1968 by Romhilt and Estes (14), and in 1973 the New York Heart Association (15). Relative sensitivity of the three methods was as follows: Total group, NYHA (77%) greater than Sokolow and Lyon (67%) greater than Romhilt and Estes (58%); Group 1, NYHA (91%) greater than Sokolow and Lyon (73%) greater than Romhilt and Estes (54%); Group 2, NYHA and Sokolow and Lyon (65%) greater than Romhilt and Estes (61%); Group 4, NYHA (79%) greater than Sokolow and Lyon (64%) greater than Romhilt and Estes (57%). We conclude that 1)ECG criteria of the NYHA for the diagnosis of LVH correlate best with an increase of ultrasonically determined septal, left ventricular posterior wall or left ventricular internal dimensions when compared with voltage criteria of Sokolow and Lyon and the point score system of Romhilt and Estes; and 2) isolated increase of left ventricular internal dimension, in the absence of thickened septum or posterior left ventricular wall, frequently results in ECG criteria compatible with the diagnosis of LVH.

The echocardiographic correlates of left ventricular hypertrophy diagnosed by electrocardiography.

Echocardiography was performed in 28 consecutive patients who manifested accepted criteria for left ventricular hypertrophy on their electrocardiograms. Four groups of patients were identified: Group 1, nineteen (68%) who had an increase in both interventricular septal and left ventricular posterior wall thickness; Group 2, three patients (11%) with isolated enlargement of the left ventricular internal dimension; Group 3, two subjects (7%) with increased septal thickness, left ventricular posterior wall thickness and left ventricular internal dimension and Group 4, four patients (14%) with normal echocardiographic measurements. It is concluded that increases in both septal and left ventricular wall thickness are the primary echocardiographic correlates of left ventricular hypertrophy as diagnosed on the electrocardiogram.

Mitral valve prolapse in patients with coronary artery disease. Echocardiographic-angiographic correlation.

Echocardiography was performed in 25 consecutive patients with angina pectoris and angiographically demonstrable coronary artery disease. Left ventricular echograms detected late or pansystolic mitral valve bowing suggesting of mitral valve proplapse in 6/25 (24%). Left ventricular angiography showed prolapse of the posterior mitral leaflet in 15/25 (60%), including 5 detected by echocardiography. Significant triple vessel coronary disease was present in 11 of 15 patients with prolapsed mitralvalve. In each of the latter a greater than 90 per cent obstructive lesion was noted in at least one coronary artery: right coronary artery, 9 subjects (82%); left circumflex coronary artery, 5 patients (33%); and left anterior descending coronary artery, 4 patients (27%). Of 15 subjects with angiographic evidence of mitral valve prolapse, 13 had left ventricular asynergy-inferior or inferoposterior in 8 subjects (62%) and anterior or anteroapical in 5 subjects (38%). Eleven subjects had vectorcardiographic evidence of transmural myocardial infarction-inferior or inferoposterior in 9 (82%) and anteroseptal in 2 (18%). A single subject with mitral valve prolapse had mild mitral regurgitation. It is concluded that: (1) coexisting prolapse of the posterior mitral valve leaflet and coronary artery disease is usually associated with triple vessel obstructive lesions, (2) severe right coronary disease, inferior left ventricular wall asynergy, and inferior myocardial infarction are important angiographic and vectorcardiographic correlates, and (3) echocardiography will detect such mitral valve prolapse in only one-third of affected cases.

Simultaneous left ventricular echocardiography and aortic blood velocity during rapid right ventricular pacing in man.

Left ventricular echocardiograms and phasic instantaneous Doppler aortic blood velocities were simultaneously recorded during short paroxysms of rapid right ventricular pacing in 20 conscious subjects. Right ventricular pacing at rates of 100, 120, 140, 160 and 180/min produced stepwise reductions of mean estimates for diastolic (D) and systolic (S) left ventricular internal dimensions (LVID) along with a diminution of aortic blood velocity. Mean (X +/- 1 standard deviation) per cent decline of LVID-D, LVID-S and peak aortic blood velocities for the study group ranged from 8.9 +/- 6.1, 8.5 +/- 5.7 and 13.7 +/- 7.7 at 100 beats/min to 29.3 +/- 10.6, 25.2 +/- 10.5 and 55.2 +/- 13.1 at 180 beats/min, respectively. When LVID-D, LVID-S, and aortic blood velocity X % reductions were plotted for all heart rates there was a high degree of positive correlation (r = 0.99). Two types of abnormal septal motion were observed during rapid pacing: Type I--paradoxical septal motion at all pacing rates (n = 7, 6/7 with left coronary artery disease); Type II--hypokinetic septal motion at lower pacing rates with flat or paradoxical motion at rates greater than 140/min (n = 13, 10/13 with normal coronary arteries). It is concluded that short episodes of rapid right ventricular pacing result in reduced LVID and abnormal septal motion with the latter possibly related to septal ischemia. Such study provides insight into the untoward influence of rapid ventricular rhythms on cardiac performance.