Two-vessel PTCA of single anomalous coronary artery.
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Biomedical subjects
Publications and source records attributed to E Grenadier.
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BACKGROUND: To assess the extent and nature of the dysfunction surrounding aneurysms of the left ventricle (LV), we examined the parameters of local and global three-dimensional shape, size, and function of LVs of eight patients with histologically confirmed anterior fibrous aneurysms. METHODS AND RESULTS: Three-dimensional reconstructions of each LV were made from 10-12 short-axis fast cine-angiographic computed tomography (cine-CT) slices encompassing the entire heart at end diastole and end systole. Regional three-dimensional wall thickness, thickening, motion, curvature, and stress index were calculated for 84 elements encompassing the entire LV. The aneurysmal border was defined by a sharp decrease in end-diastolic wall thickness and separated the LV into an aneurysmal zone and a normal zone that was further divided into adjacent normal (AN) and remote normal (RN) zones. As expected, thickening was negligible in both the aneurysmal and the border zones. Although both the AN and the RN zones had normal wall thickness (1.05 +/- 0.20 and 1.09 +/- 0.20 cm, respectively), thickening was depressed in the AN (0.22 +/- 0.08 cm) but not the RN (0.44 +/- 0.19 cm) zones. The size of the dysfunction zone (defined as less than 2 mm thickening) was found to be considerably greater than the anatomic size of the aneurysm (60.9 +/- 13.7% versus 33.6 +/- 7.6% of the left ventricular endocardial area, respectively; p less than 0.001). In addition, the AN zone had a smaller curvature and a higher stress index than the RN zone. CONCLUSIONS: LVs with fibrous aneurysms are characterized by a relatively large region of nonfunction that encompasses the thin aneurysmal area and its transitional border zone, a normally functioning remote zone, and an intermediate region of normal wall thickness but with reduced function, which may be attributed to its low curvature and high stress index.
The diagnostic and prognostic value of the oral dipyridamole test using echocardiography was evaluated in 47 consecutive patients undergoing coronary arteriography. The results of the tests were not communicated to the physicians treating the subjects during a 1-year follow-up. The test had a sensitivity of 54% and a specificity of 100% for predicting severe (greater than or equal to 70% luminal stenosis) coronary artery disease. Neither ST-T segment changes nor chest pain during the test were associated with the presence of severe coronary artery disease. In the subgroup of 34 patients with severe coronary artery disease, the appearance of left ventricular segmental systolic dysfunction or ST-T segment depression (greater than or equal to 1 mm) during the test has a strong predictive value for subsequent cardiac events during a 1-year follow-up.
Homozygous familial hypercholesterolemia (HFH) is a very rare autosomal dominant disease characterized by accelerated severe atherosclerosis. We examined 18 patients from 9 families with HFH. The age range was 6-30 years (mean = 16 years). Male to female ratio was equal. All patients had huge, multiple tuberous xanthomas on the skin and tendons. Mean +/- standard deviation of plasma cholesterol, triglycerides, low-density lipoproteins (LDL), and high-density lipoproteins (HDL) cholesterol levels were 608 +/- 89, 122 +/- 39, 550 +/- 88, and 26 +/- 8 mg/dl, respectively. Five patients (28%) had angina pectoris, two sustained a myocardial infarction, and one died at the age of 15 years. Two-dimensional echocardiography demonstrated supravalvular aortic stenosis in 3 of the 13 patients (23%). Coronary arteriography performed in 11 patients demonstrated significant obstruction in 6 patients, 2 each with single-, double-, and triple-vessel disease. Left main stenosis was present in 3 patients (27%). Supravalvular aortic narrowing was demonstrated in 6 patients (54%) and was associated with a gradient in 2 (25 and 35 mmHg, respectively). Segmental contraction abnormalities were detected in 2 of the 11 patients (18%). It is concluded that coronary artery disease is prevalent in patients with HFH and, based on the data presented, we recommend the performance of noninvasive technique, coronary arteriography and supravalvular aortography at an early age to detect and to follow the progression of the disease.
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The aims of our study were to assess the differences between plasma lipoproteins separated from five angiographically normal subjects and five patients with proven CHD. The patients with CHD had significantly higher levels of LDL-cholesterol and apo-B, and reduced levels of HDL-cholesterol and apo-Al. The biological characteristics of LDL and HDL from both groups of patients demonstrated that the LDL from the CHD patients enhanced platelet aggregation and increased cholesterol content and cholesterol esterification in MPM compared to the normal patients. HDL had no significant effect on MPM; however, there was an increased platelet aggregation with HDL derived from the CHD patients, while the HDL from the normal group decreased platelet aggregation. The data suggest that lipoproteins isolated from CHD patients are more atherogenic than lipoproteins from normal patients.
We studied the biochemical and biological properties of plasma lipoproteins taken from blood derived from either the aorta or femoral vein of patients with normal coronary arteriography. There were no significant differences in concentrations of cholesterol, triglycerides, apoprotein A-1 and apoprotein B derived from either source. The cholesterol content of very low density lipoprotein (VLDL) and high density lipoprotein (HDL) was similar in both aortic and venous blood. The low density lipoprotein (LDL) concentration, however, was significantly higher in the aortic blood sample. Arterial LDL significantly enhanced in vitro platelet aggregation when compared to venous LDL. (p less than 0.02). When incubated with mouse peritoneal macrophages (MPM) arterial LDL and VLDL caused an increased cholesterol accumulation and enhanced cholesterol esterification within these macrophages. The venous lipoproteins had little effect. The differences noted in the arterial lipoproteins in composition and biological function when compared to venous lipoproteins might be related to the much higher incidence of atherosclerosis found in the arterial tree.
A procedure for automatic sorting of three-dimensional (3-D) shapes is proposed. The procedure is applied to sort into normal and abnormal categories, human left ventricles (LV) using in vivo data from 19 subjects (ten normal and nine abnormal LV's) studied by ultrafast tomography (Cine-CT). The procedure starts by utilizing a vector in a helical coordinate system to describe the spatial geometry of each individual LV cavity. This individual vector is then anatomically aligned and normalized to eliminate effects due to size, yielding a dimensionless vector, denoted as "geometrical cardiogram" (GCG). The GCG characterizes the instantaneous 3-D geometrical information of the individual LV. For the group of healthy subjects, the Karhunen-Loeve Transform (KLT) is then applied to compress the geometric information contained in their individuals' GCG vectors, at end diastole (ED) and end systole (ES), and yield a unique set of basis vectors. The "normal shape domain" is next defined as a truncated set of the KLT basis vectors from which a normal GCG can be reconstructed with a mean squared error (MSE) smaller than a defined threshold. The calculated MSE of any individual GCG reconstructed in this domain is then used as a criterion for sorting the 3-D shapes. Hearts which yield MSE greater than the threshold are considered abnormal. When applied to the study group of 19 subjects a significant difference (p less than 0.0001) between the MSE values obtained for the normal LV's, and those obtained for the abnormal LV's was detected, thus leading to a successful sorting of all the studied LV's. Finally, the KLT is applied to yield a compact representation of the 3-D geometry of any LV (normal or abnormal).
The levels of von Willebrand factor (vWF:Ag) were measured in 27 patients with mitral valve prolapse (MVP) and compared to 27 age matched controls. Decreased levels of vWF:Ag (less than 80%) were found in 59% (16/27) of those with MVP compared to only 7% (2/27) of the controls (p less than 0.001). Mean vWF: Ag levels were also significantly lower in those with MVP (68 +/- 30% versus 100 +/- 23%, p less than 0.001). In those with MVP and congestive heart failure secondary to rupture chordae tendineae, however, the mean level of vWF: Ag was not significantly different from control values (95 +/- 32). There was an increased incidence of recurrent nose bleeds in those with MVP and low levels of vWF:Ag. We conclude that there is a relationship between MVP and low levels of vWF:Ag which may explain the increased incidence of epistaxis in such patients. Increased release of vWF:Ag in those with MVP and concomitant congestive heart failure may account for the normal levels found in this subgroup.
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Recent studies have demonstrated elevations of von Willebrand Factor following acute myocardial infarction (AMI). In order to determine if this parameter may serve as a marker for AMI, we tested the blood levels of vWF and Factor VIII:C in 28 patients with AMI, 9 patients with unstable angina, 7 patients with atypical chest pain, and 25 healthy volunteers. The level of ristocetin cofactor activity of vWF was between 70 and 144% in the control group. In patients with AMI, the mean level of this activity was 175% on the first day following infarction, rose to a peak of 270% on the fifth and sixth days, and was still significantly greater than normal in all patients on the 14th day. The vWF:Ag level closely paralleled the rise of ristocetin cofactor activity of vWF, with a peak of 336% on day 5. FVIII:C was not significantly changed. No significant elevation of vWF was observed in patients with unstable angina. The ristocetin cofactor activity of vWF and vWF:Ag thus are sensitive biochemical indicators for recent AMI, and may serve as useful markers for up to 14 days following infarction, when the traditional enzymes have returned to normal levels.
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In this study, we performed 512 echocardiographic studies on 264 consecutive unselected patients with the idiopathic mitral valve prolapse syndrome. Twenty-eight patients (10.6%) had evidence of ruptured chordae tendineae of the mitral valve on M-mode examination and in 24 the diagnosis was confirmed by two-dimensional echocardiography. Mild to severe mitral insufficiency was proven in all of them by left ventriculography during cardiac catheterization. Eight patients underwent surgery to relieve symptomatic severe mitral regurgitation. At operation all had myxomatous degeneration of the mitral valve, two patients were found to have rupture of anterior mitral chordae, and six had rupture of posterior mitral chordae. Twenty (71%) patients with chordal rupture had either mild symptoms or were completely asymptomatic. It is concluded that chordal rupture in patients with the mitral valve prolapse syndrome may be present in asymptomatic patients and go undetected clinically in a substantial number of patients unless a high index of suspicion is maintained. Serial M-mode and two-dimensional echocardiographic studies are of importance in identifying the progression of prolapse findings and may reveal the natural history of this pathologic condition in asymptomatic patients.
Polymorphous ventricular tachycardia (VT) is thought to be uncommon in acute coronary heart disease, but its prevalence has not been determined. Seven hundred seventy-one consecutive patients admitted with acute myocardial infarction (MI) were reviewed for the occurrence of this arrhythmia. Nine patients (1.2%) had polymorphous VT. No patient had any of the predisposing factors previously associated with polymorphous VT. The arrhythmia was resistant to multiple drugs, and repeated cardioversion was effective in only 3 patients. Overdrive pacing was ineffective in the 3 patients in whom it was attempted. Verapamil was effective in 3 of 4 patients in whom it was tried. Six patients with polymorphous VT died during hospitalization; the remaining 3 died within 6 months of discharge. It is concluded that, when compared with regular VT, polymorphous VT in MI carries a poor prognosis. When the arrhythmia occurs in the context of acute ischemia, it appears to be more difficult to treat compared with its occurrence due to other predisposing factors. Verapamil, not usually indicated for ventricular arrhythmias, should be tested in a therapeutic trial.
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