Citations

The contributions of histamine (H1 or H2) receptor-mediated responses and, therefore, the effects of histamine blocking agents are unclear with regard to regulation of proximal epicardial and distal resistance coronary arteries. This study was designed to evaluate the effects of selective H1- and H2-receptor antagonists on epicardial and resistance vessels in the closed chest dog model. Histamine, diphenhydramine (H1 blocker), and cimetidine (H2 blocker) were infused into the left anterior descending coronary artery (LAD), and responses were studied by quantitative coronary angiography and flow measurements (133Xe washout). Histamine infusion alone produced a significant dilation of the proximal LAD (13% above control) only at the highest dose (45 micrograms/min), while LAD flow was increased by 128%. In the presence of H1 blocker, histamine produced significantly greater epicardial dilation (55% above control). The flow response curve was shifted to the right in the presence of H1 blocker, but the flow attenuation was overcome by the highest histamine dose. In contrast, the H2 blocker attenuated both epicardial dilation (6% below control) and flow response (31% above control) to the highest histamine dose. Results support a differential regulation of proximal epicardial and distal resistance vessels to histamine with epicardial arteries demonstrating H1-mediated vasoconstriction and H2-mediated vasodilation and distal resistance vessels showing H1- and H2-mediated vasodilation. In addition, these findings suggest that H1 blockade may antagonize histamine-related vasoconstriction and vasospasm, while H2 blockers may permit unopposed H1-mediated vasoconstriction of epicardial arteries and also limit resistance vessel vasodilatory responsiveness in the presence of elevated tissue histamine, as may occur in atherosclerotic coronary artery disease.

Background —Left ventricular ejection fraction (LVEF) is a recognized determinant of survival in patients with coronary artery disease. In major trials comparing surgical and percutaneous revascularization approaches, the long-term effect of the coronary revascularization strategy on LVEF has not been reported. Methods and Results —In the NHLBI-sponsored Bypass and Angioplasty Revascularization Investigation (BARI) randomized trial comparing angioplasty and bypass surgery as initial treatment strategies, 1220 (75%) of the 1617 surviving randomized patients had their EF measured by radionuclide ventriculography 5 years after study entry. For the total study group, the 5-year EF in the CABG group (n=623) was 55.8±12.3, compared with 55.7±12.7 in PTCA group (n=597, P =0.82). There was no significant difference in measured EF between the CABG group and the PTCA group within multiple subgroups determined by the presence or absence of diabetes, 3-vessel disease, complete revascularization, or prior myocardial infarction. In a multiple linear regression model developed to predict 5-year EF, treatment assignment to PTCA or CABG was not significant ( P =0.95). If an EF of 0 was imputed for patients who were dead and missing EF data, however, there was a higher EF in the CABG group ( P =0.0018) among diabetic patients only. Conclusions —In the BARI randomized trial, initial treatment assignment to angioplasty was not associated with any difference in long-term ventricular function compared with initial treatment assignment to surgery. These results apply, however, only to patients who were alive at 5 years.

BACKGROUND Normal Doppler hemodynamics for tricuspid prostheses have not been well characterized in a large group of patients. Therefore, we analyzed comprehensive Doppler echocardiographic examinations of 82 patients with tricuspid prostheses that were normal by clinical and two-dimensional echocardiographic examinations to establish the normal hemodynamics of various types and sizes of tricuspid prostheses. METHODS AND RESULTS The earliest complete postoperative echocardiographic study from each patient was chosen for analysis. Doppler examinations were analyzed on an off-line station from tapes or Doppler strip charts. Early velocity, atrial velocity, end-diastolic velocity, pressure half-time, and mean gradient were obtained by digitizing tricuspid velocity curves. The incidence of "physiological" tricuspid prosthetic regurgitation was noted. Ten Doppler cycles were measured for each patient, and maximal, minimal, and average measurements were recorded. The mean values +/- SD of early velocity, atrial velocity, end-diastolic velocity, mean gradient, and pressure half-time and incidence of mild prosthetic regurgitation were reported for each type of prosthesis, as were highest Doppler measurements for each valve type. Average pressure half-time was significantly lower for St Jude than for heterograft prostheses (P = .04). There were no significant differences between the valve types for mean gradient, early velocity, or incidence of prosthetic regurgitation. Increasing prosthesis size was associated with lower average pressure half-time for heterograft prostheses (P = .024). Average differences (respiratory- and cycle-length-dependent) between maximal and minimal values for 10 cardiac cycles were established for each prosthesis. CONCLUSIONS This study establishes normal ranges for Doppler hemodynamics of various tricuspid prostheses and emphasizes the importance of measuring multiple cycles for each tricuspid prosthesis, regardless of cardiac rhythm.

BACKGROUND Maroteaux-Lamy syndrome is a lysosomal storage disease of mucopolysaccharide metabolism (MPS type VI) that may involve the mitral and aortic valves. Affected patients have other skeletal and oropharyngeal malformations that complicate anesthetic and surgical management. METHODS AND RESULTS The present report describes the clinical, echocardiographic, and pathological findings in four patients with Maroteaux-Lamy syndrome. Two of three siblings underwent successful double-valve replacement for aortic and mitral valve stenoses. The third sibling, whose aortic and mitral valves were thick and fibrotic, died from septicemia after hip surgery. A fourth, unrelated patient also had successful double-valve replacement. CONCLUSIONS Our experience emphasizes the potential difficulties in preoperative assessment and surgical treatment as well as the unique problems related to airway management in patients with this syndrome.

BACKGROUND Transthoracic Doppler echocardiography examination has become an integral part of the investigations performed in patients with mitral valve prostheses. The limitations of the transthoracic approach are well documented. Transesophageal echocardiography provides a unique window for achieving a clear view of the mitral prosthesis. METHODS AND RESULTS This study shows the usefulness of transesophageal echocardiography in clinical practice for assessment of patients with a mitral valve prosthesis. This technique demonstrated an abnormality in 48% of patients who had normal results on transthoracic examination. The overall sensitivity of transesophageal echocardiography was 96%. CONCLUSIONS Transesophageal echocardiography constitutes an essential part of a comprehensive two-dimensional/Doppler echocardiographic examination in patients with suspected malfunction of mitral prostheses.

The effect of valvular insufficiency on left ventricular volumes was studied by an angiographic method in 37 patients. Ejection of the additional volume load imposed by valvular insufficiency was achieved by an increase in end-diastolic volume and not by increasing the proportion of end-diastolic volume ejected. Of the 37 patients, 16 (43 per cent) had a significant reduction in the fraction of end-diastolic volume ejected per beat. These patients performed significantly less stroke work from a given end-diastolic fiber length (end-diastolic volume) than did the others and evidence is presented that they had impaired myocardial function. An index of myocardial contractility is derived which relates stroke work to end-diastolic volume. The magnitude of left ventricular volumes is determined in part by the severity of the volume load but a further increase in volume without necessarily a further increase in ejection occurs in those patients with impaired myocardial function. Valvular insufficiency is quantitated from the difference between left ventricular ejection volume determined angiographically and forward stroke volume determined from indicator-dilution curves. The results show good agreement with subsequent surgical findings in the 15 patients who underwent operation.

Left heart volumes were determined angiographically in 50 subjects of whom 18 had no abnormality of the left heart, 12 had lesions causing pressure overload of the left ventricle, and 20 had lesions causing volume overload of the left ventricle. The left heart volumes were in the normal range in the presence of pressure overload, but, with volume overload, end-diastolic, end-systolic, and atrial volumes were in excess of normal. A linear relationship was demonstrated between end-diastolic and end-systolic volumes, regardless of the pressure load on the ventricle. Thus, for all but one of the cases studied, total left ventricular ejection volume formed a nearly constant proportion of end-diastolic volume.

Clinical, hemodynamic, and angiocardiographic findings are described in seven cases of congenital mitral insufficiency. The volumes and changes in volume of the left atrium and left ventricle were calculated from the angiocardiograms and were found to be increased above the range of normal. Left ventricular stroke volumes thus obtained were compared with forward flows calculated from indicatordilution curves in order to quantitate regurgitant flow. Regurgitant flows varied between 19 and 94 per cent of the total left ventricular ejection volume, and forward flow was maintained as a result of a considerable increase in left ventricular volume. The left ventricular ejection volume was 50 to 64 per cent of the end-diastolic volume.

The purpose of this investigation was to study the incidence and location of systemic arterial occlusion and pulmonary embolism in a consecutive series of cases of fatal acute myocardial infarction. Another consecutive series of cases in which healed myocardial infarction was demonstrated at necropsy was similarly studied. In none of the cases included in this study had anticoagulant therapy been employed. Massive pulmonary embolism was the most frequent fatal thrombo-embolic complication found among the cases of acute myocardial infarction. Cerebral infarction was the most frequent fatal thrombo-embolic complication found among the cases of healed myocardial infarction. Cerebral infarction was the most frequent fatal systemic arterial thrombo-embolic lesion in both groups. Acute splenic and renal infarcts were frequently demonstrated but with one exception appeared to play an incidental role in the clinical course of the patients. Although systemic arterial occlusion was frequently found in association with intracardiac mural thrombi, there were many other cases in which evidence of systemic arterial occlusion was found in the absence of intracardiac mural thrombi. A positive correlation existed between the presence of pulmonary and systemic arterial occlusion and the occurrence of congestive cardiac failure.

This is a study of the location and incidence of intracardiac thrombi in acute and in healed myocardial infarction. In myocardial infarction intracardiac thrombi occur predominantly in the left ventricle. Anterior myocardial infarcts are more commonly associated with mural thrombi than posterior myocardial infarcts. Large myocardial infarcts and congestive failure are factors which predispose to the formation of left ventricular mural thrombi in myocardial infarction.