The aetiology and course of isolated severe aortic regurgitation: a clinical, pathological, and echocardiographic study.

Seventy two consecutive patients with severe isolated aortic regurgitation were evaluated by preoperative echocardiographic and angiographic assessment of the aortic root. Biopsy specimens of the aortic wall were taken at operation. Two major groups of patients were found: those with cusp derangement but normal aortic roots and those with normal cusps but dilated aortic roots. Of the 42 cases of abnormal cusps, 20 were rheumatic, 15 were infective, and six were bicuspid. One patient had a tear in an otherwise normal cusp. Of the 30 cases of abnormal roots but normal cusps, six had inflammatory changes (syphilis, Reiter's disease, giant cell aortitis) and 24 had root dilatation caused by non-inflammatory destruction of elastic laminae. Echocardiographic measurement of the aorta at the level of the top of the commissures predicted the findings at pathology. In 37 of 39 patients with cusp disease the measurement was less than 37 mm. In 27 of 33 patients with root disease the measurement was greater than or equal to 37 mm. This difference was statistically significant. There was no difference in the sizes of the prosthesis used in each group, suggesting that it was the diameter of the junction of the aorta with the sinuses rather than the junction of the sinuses with the ventricle that was important in aortic regurgitation. Clinical progression in patients with non-inflammatory aortic root disease is slower than in patients with infective disease but faster than in those with rheumatic cusp disease.

Inappropriate left ventricular hypertrophy in minor aortic valve disease: a source of error in clinical assessment.

A group of patients with minor aortic valve disease and inappropriately severe left ventricular hypertrophy is described. Clinical, electrocardiographic and echocardiographic assessment of the degree of left ventricular hypertrophy suggested that they had haemodynamically severe aortic stenosis but this was not borne out at cardiac catheterisation. Although a chance association between non-obstructive hypertrophic cardiomyopathy and mild aortic stenosis may have been responsible, an abnormally severe hypertrophic response to minor aortic outflow obstruction is proposed as another possible explanation. The association between minor aortic valve disease and severe left ventricular hypertrophy should be considered when assessing aortic stenosis since the prognosis with medical management seems good and valve replacement is likely to be of no benefit in such cases.

The loud first heart sound in left atrial myxoma.

The interrelation between the loudness of the first heart sound, the time interval from the Q wave to the onset of the first heart sound (QM1), and the mitral valve closure rate was studied in nine patients presenting with left atrial myxomata. In seven patients the first heart sound was loud preoperatively and was associated with delayed mitral valve closure. After removal of the myxoma the onset of mitral valve closure returned towards normal, the mitral valve closure rate was reduced, and the first heart sound became softer. In two patients the first heart sound was normal before and after operation as were both the time of onset of mitral valve closure and the mitral valve closure rate. In neither of these patients did the myxoma completely fill the mitral orifice during diastole. The loud first heart sound in left atrial myxoma is a useful clinical sign, and intensity is directly related to the delay in onset of closure of mitral leaflets.

Changes in echocardiographic left ventricular minor axis dimensions during exercise in patients with aortic stenosis.

Twelve patients with aortic stenosis (gradient 62 (25) mm Hg), and six normal subjects were examined using M mode echocardiography before and during submaximal bicycle exercise. Normal subjects showed a progressive fall in the end systolic minor axis dimension of the left ventricle and a rise in end diastolic dimension, giving an increase in stroke dimension and shortening fraction of 45% and 37% respectively at peak exercise. Patients with aortic stenosis showed no consistent alteration in either end systolic or end diastolic dimension, and consequently stroke dimension was unchanged during exercise. None of the patients with an abnormal exercise response had evidence of left ventricular failure at rest, and all but one completed the exercise protocol without undue dyspnoea. Non-invasive exercise testing in patients with aortic stenosis may detect abnormalities of left heart function which are not apparent at rest. These abnormalities may provide early evidence either of severe aortic stenosis or of incipient left ventricular failure.

Comparison of cinefluoroscopy and M mode echocardiography for detecting aortic valve calcification. Correlation with severity of stenosis of non-rheumatic aetiology.

The density of aortic valve calcification was estimated using cinefluoroscopy and M mode echocardiography in 86 patients with pure aortic stenosis. The results were compared with the degree of outflow obstruction measured haemodynamically. Cinefluoroscopic estimates of aortic valve calcification correlated well with the measured aortic valve gradient whereas echocardiographic results were less accurate. Echocardiography gave accurate information about the distribution of calcium within the cusps, but this was not of value in predicting the degree of obstruction. The amount of calcium in the aortic valve as assessed by simple cinefluoroscopy is a useful guide to the severity of aortic stenosis in patients in the middle and older age groups.

Significance of complete right bundle-branch block when an isolated finding. An echocardiographic study.

Twenty-seven patients with complete right bundle-branch block as the only abnormal finding were studied using high speed M-mode echocardiography to determine the effect of the electrical delay on the mechanical events of right ventricular systole. Pulmonary valve opening (PVOm) was delayed in all cases. In some the delay was mainly between mitral valve closure (MVC) and tricuspid valve closure (TVC), and this was designated proximal block. In the others the main delay was between tricuspid valve closure and pulmonary valve opening and this was designated distal block. The patients were divided into those with proximal and those with distal block by calculating the ratio TVC-PVOm/MVC-TVC. Twelve out of 13 of those with distal delay but only one out of 14 of those with proximal delay had episodes of syncope or near syncope. These results are consistent with previous theories about the pathophysiology of right bundle-branch block. Echocardiography may offer a non-invasive method to estimate the prognosis in isolated right bundle-branch block.

Unsuspected coronary artery disease as cause of chronic atrioventricular block in middle age.

Attention has recently been drawn to the relatively poor prognosis of middle aged patients paced for chronic atrioventricular block when age-linked expectation of life is taken into account, and it has been suggested that this may be the result of underlying coronary artery disease, despite the absence of symptoms to suggest this. It was the purpose of this study to determine the incidence of unsuspected coronary artery disease in middle aged patients presenting with chronic atrioventricular block. Studies were made on a consecutive series of 30 patients aged 45 to 65 (mean age 56 years) with chronic atrioventricular disease who had been referred for pacing. Patients presenting with acute myocardial infarction or angina or with sinuatrial disease without atrioventricular disease were excluded. Coronary arteriography disclosed the presence of severe coronary artery disease in 13 patients. Of the remaining 17 patients, four had congestive cardiomyopathy, two had hypertrophic cardiomyopathy, one had aortic stenosis, and in 10 patients the aetiology of the heart block was unknown. Myocardial revascularisation was undertaken in six patients with paroxysmal atrioventricular block caused by coronary artery disease. Operation did not result in any sustained improvement in atrioventricular conduction.

Non-invasive diagnosis of subpulmonary outflow tract obstruction.

We have studied the echocardiographic and phonocardiographic findings in 18 patients with obstruction to ventricular outflow at subpulmonary valve level. The aetiology was congenital in 13 patients, a result of hypertrophic cardiomyopathy in three, and infiltration of the right ventricular outflow tract by glycogen or lymphoma in the remaining two. Abnormal systolic motion of the pulmonary valve, fluttering, and early or midsystolic closure were seen in 16 of 17 patients in whom the cusps were visualised. Normal pulmonary valve motion was found in one patient with coexisting pulmonary valve stenosis. In congenital infundibular stenosis the delay of the pulmonary component of the second heart sound (P2) was related to the severity of the obstruction. A pulmonary ejection sound, defined as a high-frequency sound occurring at the moment of full pulmonary valve opening, was absent except in the patient with coexisting pulmonary valve stenosis. In hypertrophic cardiomyopathy with obstruction to the right ventricular outflow, the ejection systolic murmur was softer with inspiration, a finding that contrasts with the respiratory variation seen with fixed obstruction. Recognition of these abnormalities should allow an accurate non-invasive diagnosis to be made and permit assessment of severity when P2 can be recorded.

Septicemia in patients with an endocardial pacemaker.

The records of 1,235 consecutive patients treated with long-term pacing by the endocardial route between 1964 and 1977 were analyzed to determine the incidence, mechanism, course and treatment of septicemia. Septicemia developed in 12 patients (1 percent), and Staphylococcus aureus was isolated from the blood culture in 10. All patients were treated with the usual prolonged course of bactericidal drugs. Treatment was successful in only two of the seven patients whose endocardial pacing system was left in place; in three of the seven the septicemia recurred, necessitating removal of the endocardial system, and two of these patients died. In the remaining four patients the endocardial wire was promptly withdrawn, with use of a thoracotomy when necessary, and an epicardial system inserted; all of these patients survived. This is the treatment of choice.

Prognosis of patients paced for chronic atrioventricular block.

Between the years 1960 and 1974, 839 patients were paced for chronic complete atrioventricular block. Analysis of survival compared with the general population showed that 170 deaths were expected according to standard mortality tables and 288 actually occurred, giving a ratio of actual to expected deaths of 1.7:1. Patients with a definite history of myocardial infarction showed a higher than average mortality when paced. Mortality was not influenced whether heart was constant or intermittent, whether the ventricular rate was below or above 40/minutes, or whether QRS duration was greater or less than 0.1 second. Analysis of the age groups paced disclosed the most important correlations. Between the ages of 80 and 89 years paced patients could expect to survive as long as other of the same age without heart block. There was, however, a very high ratio of 4.5:1 for 90 patients in the age group 50 to 59 years. The reason for the high mortality ratio was uncertain but it may have been the result of a greater incidence of underlying coronary artery disease.