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Left ventricular wall motion abnormalities, the extent and location of coronary artery stenoses, and the radiographic evidence of pulmonary venous hypertension were analyzed in a retrospective study of 40 patients who had surgically proven rupture of the interventricular septum after myocardial infarction. In 33 patients in whom chest films were available, interstitial or alveolar pulmonary edema was present in 78%, while left ventricular enlargement was present in 82%. Of 26 patients who had coronary angiography, complete occlusion of the right coronary artery, left anterior descending artery, or left circumflex artery was present in 92%, with few, if any, collateral vessels around the occlusion. The location of the rupture in the muscular septum was always in the region of akinesis or dyskinesis. Posterior defects were associated with posterobasal and diaphragmatic akinesis, and anterior defects with apical akinesis. Left ventricular aneurysms were adjacent to the septal rupture in 68%, and 74% had mitral regurgitation. The right ventricular diaphragmatic wall in posterior rupture was always akinetic, indicating right ventricular infarction. Thus ventricular septal defect after myocardial infarction (1) tends to occur with multiple coronary occlusions about which little collateral flow develops; (2) can accurately be localized anteriorly or posteriorly in the muscular septum by the location of the akinetic left ventricular wall segment; and (3) has an associated right ventricular infarct when rupture is posterior.
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PMID:Coronary, ventricular, and pulmonary abnormalities associated with rupture of the interventricular septum complicating myocardial infarction. 10 43

The clinical, hemodynamic, and angiographic findings were correlated with the heart size in 207 patients with proved coronary artery disease. Cardiomegaly was noted in 34 patients and normal heart size in 173. In these two groups, the patients' age range, duration of disease, and history of myocardial infarction were similar. There was no statistical difference in incidence of shortness of breath, hypertension, left ventricular hypertrophy, or abnormal glucose tolerance. Patients with cardiomegaly had a significantly higher incidence of congestive heart failure (26 per cent) as compared to patients with normal heart size (2.9 per cent) (P less than 0.001). Patients with enlarged heart presented a high incidence of anterior wall or multiple myocardial infarction (73 per cent) (P less than 0.001). The cardiomegaly group had a high incidence of elevated end-diastolic volumes, elevated end-diastolic pressures, and diminished ejection fractions when compared to patients with normal heart size (P less than 0.01). Double and triple coronary artery disease was more frequent in patients with cardiomegaly and total coronary score was also higher in this group (P less than 0.005). Asynergy was present in 55 per cent of patients with normal heart size but in 82 per cent of those with enlarged hearts (P less than 0.01). The group of patients with cardiomegaly and documented congestive heart failure had ejection fractions less than 0.30. Cardiac catheterization is probably not advisable in these patients in the absence of associated significant mitral regurgitation, ventricular septal defect, or ventricular aneurysm.
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PMID:Correlation of heart size with clinical and hemodynamic findings in patients with coronary artery disease. 12 83

Mitral reguritation is a relatively common finding in coronary heart disease. In this series of 127 patients, selected with a view to coronary or left ventricular surgery on the basis of severity of symptoms, the incidence was 39 (31%). Mitral regurgitation is significantly more common in patients with a history or electrocardiographic evidence of previous myocardial infarction. Clinically it may present as a pan- or late systolic or even a mid-systolic, ejection type murmur at the apex or at the left sternal edge; but in 39 per cent of the patients with angiographic mitral regurgitation no murmur was present. Angiographically important mitral regurgitation (grades 2-4/4) was usually associated with a systolic murmur; this finding was independent of ejection fractions. Left ventricular enlargement clinically or radiographically is likely to accompany mitral regurgitation but left atrial enlargement (electrocardiographically or on chest x-ray) is a more reliable pointer to mitral regurgitation and pulmonary venous hypertension is even more strongly suggestive of its presence. The electrocardiographic signs of papillary muscle infarction were rare in this series (15%) and were not related to angiographic mitral regurgitation. There was no difference in the incidence of mitral regurgitation in association with anterior or inferior myocardial infarction or in distribution of coronary artery disease. There is, however, a higher incidence of mitral regurgitation in more severe coronary arterial disease (P less than 0-05). The incidence of mitral regurgitation is significantly higher with reduction in left ventricular ejection fraction (P less than 0-001), with rise in the left ventricular end-diastolic pressure (P less than 0-02), and with abnormal contraction patterns, but the severity of mitral regurgitation is not significantly related to these findings.
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PMID:Mitral regurgitation in coronary heart disease. 13 31

Echocardiography is an extremely useful noninvasive technic in the differential diagnosis of a large heart. It may show whether a large heart is due to left ventricular hypertrophy or dilatation, or if it is due to a pericardial effusion. The hypertrophied heart may be further characterized by determining whether it is symmetrical, as caused by aortic stenosis or hypertension, or whether it is assymmetrical, which is characteristic of hypertrophic cardiomyopathy. Similarly, dilatation of the heart may be due to volume overload of the left ventricle secondary to valvular insufficiency, congestive cardiomyopathy or ischemic heart disease; these can be distinguished by echocardiography. As certain types of mitral insufficiency are associated with specific valvular dysfunction, the possible etiology of the mitral insufficiency and therefore of the volume overload of the left ventricle may be determined using echocardiography. Finally, mediastinal tumors may simulate a large heart, and demonstration of normal cardiac dimensions and wall motion can exclude a cardiac etiology for the "large heart."
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PMID:Echocardiography in the differential diagnosis of the large heart. 13 5

Sixty-two autopsied hearts, with left ventricular hypertrophy (LVH) caused by mitral regurgitation (MR), aortic failure (AR), combined valvular disease (CVD), hypertension (HHD), or ischemia (IHD), and 23 control hearts with normal left ventricles were studied morphologically for analysis of modes of hypertrophy and for ECG-pathology correlation. Basic disorders modify the mode of hypertrophy; that is, elongated AR-type LV makes muscle fiber orientation in the outer layer more vertical, and globular MR-type LV makes it more horizontal than normal. High-voltage QRS correlates with hypertrophy of the outer layer which is often associated with that of the inner layer. ST depression and T changes correspond to relative deterioration of the inner and median layers, respectively.
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PMID:Histopathological study of hypertrophied myocardium of known etiologies with special reference to correlation of ECG changes. 14 36

This report reviews the clinical features of 80 patients with roentgenographically proved mitral annular calcification. The mean age of the group was 73 years, and there was a 2.5 to 1 female to male ratio. Evaluation for underlying cardiovascular disease revealed six patients with severe calcific valvular aortic stenosis; five patients with hypertrophic cardiomyopathy, 11 with mitral prolapse and 33 with significant arterial hypertension (blood pressure greater or equal to 150/96 mm Hg). Eighty-five per cent of the group (68 of 80 patients) had an underlying cardiac disorder associated with either chronically increased left ventricular systolic pressure or abnormal leaflet motion. Other cardiovascular abnormalities occurring as complications secondary to the mitral ring calcification included subacute bacterial endocarditis (three cases), arterial emboli (five episodes) and high grade atrioventricular block (16 cases). Twelve patients had severe mitral regurgitation; successful mitral valve replacement was carried out in four patients (all with myxomatous mitral tissue). Evidence of diffuse conduction system disease, not limited to the area of the cardiac fibrous skeleton, was found frequently (44 patients). Nine patients had sinus node dysfunction and 35 patients had electrocardiographic evidence of distal intraventricular (fascicular) block. Twenty-one patients eventually required pacemakers for management of symptomatic bradyarrhythmias. Atrial fibrillation was present in 23 patients. In this review it was found that calcification of the mitral annulus is frequently associated with or induces serious cardiovascular disease. Since some of these disorders may be modified by appropriate therapy, calcification of the mitral annulus should no longer be ignored as a benign marker of the elderly heart.
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PMID:Calcification of the mitral annulus: etiology, clinical associations, complications and therapy. 15 99

The authors report a clinical and phonocardiographic study of functional aortic systolic murmurs in 26 elderly patients, in 19 of which the lesion was confirmed pathologically. Systolic murmurs radiating across the chest in elderly have the same clinical characteristics as aortic stenosis from which they may, however, be distinguished owing to the: absence of a thrill during systole. The brief duration and the proto-meso-systolic position of the murmur with early inscription of maximal oscillations on the phonocardiogram. Conversion of the second aortic sound. Almost constant absence of a diastolic murmur. Normal carotid arteriogram, including normal ejection time after correction and time of half rise. "Innocent" systolic murmurs are due to calcification of the aortic valve without stenosis, and/or dilatation of the ascending aorta. There is no systolic pressure gradient between the left ventricle and the aorta during cardiac catheterisation. No lesions were found in the mitral valve suggesting mitral incompetence, therefore, we consider the term mitro-aortic murmur used by Huchard should be dropped; Radiation of the murmur from the apex of the heart up into the neck may be explained by the simultaneous occurrence of anatomical changes due to age and/or hypertension and by the vibratory nature of the murmurs which become propagated above and below their origin, as shown by the intracardiac recordings.
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PMID:[Functional aortic systolic murmurs in the elderly]. 17 95

The case files of 4,456 medical admissions in 1975--1976 at Ahmadu Bello University Teaching Hospital, Kaduna, Nigeria, included 354 cardiovascular patients. The most common causes were hypertension (45.5%), cardiomyopathy (20.6%) and chronic rheumatic heart disease (14.4%). The mean age of hypertensive and cardiovascular patients was lower than in Europe. The majority of hypertensive patients suffer from essential hypertension. Congestive cardiac failure is the commonest complication of hypertension and cardiomyopathy. Rheumatic valvular disease with mitral incompetence is frequent and sometimes severe in young people. Other cardiovascular diseases included pericardial disease, bacterial endocarditis, cor pulmonale, anaemic heart failure, congenital and syphilitic heart disease. Coronary heart disease was only encountered in non-Africans. Cardiovascular mortality in hospital was high (20%).
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PMID:Cardiovascular disease in Northern Nigeria. 31 94

Left ventricular stiffness is defined by the relationship between pressure and volume and can be altered by a variety of disorders. In disorders with high VLVED, such as mitral regurgitation, protection of pulmonary capillaries from high pressure is provided by a PV shift. In contrast, increased stiffness is produced by ventricular hypertrophy or ischemic heart disease, which puts the patient at increased risk for pulmonary capillary hypertension. Changing the ventricular PV relationship by therapy is an exciting prospect.
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PMID:Left ventricular stiffness. 34 43

The diastolic characteristics of the left ventricle with special reference to the patterns of left ventricular filling and diastolic posterior wall movement were studied echocardiographically in 95 patients with various cardiac conditions including constrictive pericarditis, idiopathic cardiomyopathy (CCM, HCM), valvular aortic stenosis (AS), mitral stenosis (MS), hypertension (HT), aortic insufficiency (AI), mitral insufficiency (MI), and in 20 normal subjects. 1. Various types and severities of LV diastolic abnormalities were revealed by analyzing the patterns of posterior wall movement and LV filling in three diastolic phases--rapid filling period, slow filling period, and atrial filling period, respectively. 2. Disturbances of posterior wall distension and LV filling during the rapid filling period with a compensatory augmentation of atrial contribution to LV filling were observed in most patients. These patients also showed a markedly decreased posterior wall velocity and LV filling rate during rapid filling period. 3. E-F slope was significantly decrease in patients with MS, AS, and HCM. E-F slope correlated well with DPWV and RFR in most patients. In MS, however, DDR decreased to a disproportionate degree with a decrease in DPWV and RFR, probably due to the structural changes and decreased mobility of the mitral valve. From this study, we conclude that the patterns of the left ventricular filling and posterior wall movement during three phases of diastole obtained by echocardiography is useful in detecting left ventricular diastolic abnormalities.
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PMID:Echocardiographic study on diastolic posterior wall movement and left ventricular filling by disease category. 45 17


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