Sheiban I

Relation of body fat distribution in men and degree of coronary narrowings in coronary artery disease

This study evaluates the relation between body fat distribution and severity of coronary artery disease (CAD). The study sample comprised 33 patients with angiographically demonstrated CAD and 10 angiographically normal control subjects. Body fat distribution was estimated by computed tomography and degree of coronary narrowings by angiographic score. Body weight, body mass index and total and subcutaneous abdominal adipose tissue areas showed no statistical differences in the 2 groups; visceral abdominal adipose tissue area and the visceral to subcutaneous abdominal adipose tissue area ratio were significantly higher in patients with CAD (p < 0.05). There was a significant correlation between visceral fat and triglycerides, apoprotein B and sum of glucose and insulin during glucose oral tolerance test. Sum of insulin during glucose oral tolerance test, visceral abdominal adipose tissue area and visceral/subcutaneous abdominal adipose tissue area ratio correlated significantly with severity of CAD, as evaluated by coronary score in all subjects and in CAD patients alone. Stepwise multiple regression analysis using the coronary score as the dependent variable and anthropometric and metabolic parameters as independent variables shows that in all subjects and in CAD patients alone, visceral/subcutaneous abdominal adipose-tissue area ratio entered the regression first and the sum of insulin during glucose oral tolerance test second. The results suggest that visceral abdominal adipose tissue area and visceral to subcutaneous abdominal adipose tissue area ratio may be cardiovascular risk factors.

Interrelation between angiographic severity of coronary artery disease and plasma levels of insulin, C-peptide and plasminogen activator inhibitor-1

Plasma insulin, C-peptide and plasminogen activator inhibitor-1 (PAI-1) levels were measured in 64 men with coronary artery disease (CAD) documented by angiography. Coronary arteriograms were analyzed, and the severity and diffusion of coronary lesions were quantified by score systems. C-peptide and PAI-1 levels in patients with CAD were significantly higher than in 30 control subjects. Insulin, C-peptide and PAI-1 showed a highly significant correlation with the severity scores for coronary lesions (C-peptide more than insulin), but only a weak correlation with diffusion scores. Highly significant correlations were found between insulin and PAI-1, and even greater ones between C-peptide and PAI-1. It has been proposed that hyperinsulinemia may be involved in the etiology of atherosclerotic cardiovascular disease by dysregulating lipoprotein metabolism and blood pressure. These findings support that hypothesis and suggest that insulin secretion may be an index of the severity of CAD. Because a direct effect of insulin on the cells that synthesize PAI-1 has been shown, the present data further indicate that the effect of insulin on fibrinolysis may be another way by which hyperinsulinemia accelerates atherogenesis.

Recovery of left ventricular function following early reperfusion in acute myocardial infarction: a potential role for the calcium antagonist nisoldipine.

The purpose of the present study was to test whether the administration of a vascular-selective organic calcium antagonist (nisoldipine) at the onset of early mechanical reperfusion (by coronary angioplasty) in acute myocardial infarction could prevent or attenuate postischemic stunning and enhance the recovery of left ventricular function in these patients. The study included 36 patients with anterior acute myocardial infarction who underwent an early and successful primary coronary angio-plasty within 3 hours of the onset of chest pain (mean time to reperfusion = 113 ± 37 minutes). The infarct-related artery was the left anterior descending artery in all patients. All had single-vessel disease. Baseline coronary arteriography was completed by left ventriculography. When the infarct-related artery was identified, a guidewire was placed into the target vessel and a balloon catheter was positioned in the artery. At this point all patients were administered 0.3 mg of intracoronary nitrates through the guiding catheter. Patients were then randomized. Seventeen patients (the NIT group) did not receive further treatment during the procedure, while the other 19 patients (the NIS group) received an additional 0.05 mg of intracoronary nisoldipine. Postprocedure treatment consisted of oral nitrates (80–120 mg/day) plus enalapril (10–20 mg/day) in the NIT group patients, and oral nisoldipine (20 mg/day) plus enalapril (10–20 mg/day) in the NIS group patients. The same treatment was maintained during the 6-month follow-up period. An echocardiographic study was performed at 1, 7, 30, 90, and 180 days following the procedure. Left ventriculography and coronary angiography were repeated at 1 and 180 days after the mechanical reperfusion. An exercise test was performed at 30, 90, and 180 days following primary angioplasty. Left ventriculograms and two-dimensional echocardiograms were analyzed by a computerized system that evaluated left ventricular volumes, ejection fraction, segmental wall motion, and diastolic function (from the left ventricular volume curve). Under baseline conditions, the clinical and angiographic characteristics of the patients were similar in both treatment groups. The results showed a significantly earlier recovery of left ventricular systolic and diastolic function in the NIS group patients compared with those of the NIT group. Also, exercise capacity was significantly better at 30 days in the NIS group. The findings of the present study provide further evidence that early reperfusion in acute myocardial infarction is likely to be followed by myocardial stunning. The vascular-selective organic calcium antagonist nisoldipine, administered at the onset of reperfusion, seems to attenuate postischemic stunning and to enhance the recovery of left ventricular function in this clinical subset.

Clinical and therapeutic implications of chronic left ventricular dysfunction in coronary artery disease.

In patients with myocardial ischemia, left ventricular dysfunction (LV) may arise from irreversible damage (cell death), myocardial stunning (postischemic dysfunction), or myocardial hibernation (persistent myocardial dysfunction at rest due to underperfusion). Chronic LV dysfunction usually refers to hibernating myocardium. However, stunning might also become chronic, producing persistent myocardial dysfunction. Clinical studies have demonstrated that many patients with coronary artery disease have subsequent recurring ischemic (symptomatic or silent) episodes at short intervals in the same area and that each episode may be followed by myocardial stunning. In these patients the myocardium may not recover fully between episodes and function may remain reversibly depressed for long periods or may even be clinically depressed. The recognition of both stunning and hibernation is very important clinically and therapeutically, since chronic LV dysfunction may have a negative effect on mortality and morbidity in patients with coronary artery disease. Moreover, both clinical states are potentially correctable. Pharmacologic intervention with beta blockers, angiotensin-converting enzyme inhibitors, or calcium antagonists might improve or protect hibernating myocardium. The acute hemodynamic effects of the dihydropyridine calcium antagonist nisoldipine have been investigated in patients with chronic LV dysfunction probably arising from hibernating myocardium. Nisoldipine was found to improve both left ventricular systolic and diastolic function without activating the adrenergic system. The improvement in systolic function may be due to a redistribution of coronary blood flow and to a slight reduction in afterload induced by nisoldipine. On the other hand, nisoldipine may improve diastolic function in these patients by an intrinsic mechanism, Reducing intracellular calcium overload or balancing intracellular calcium homeostasis in the ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)

Two-dimensional echocardiography in the diagnosis of intracardiac masses: a prospective study with anatomic validation

The accuracy of two-dimensional echocardiography in the detection of intracardiac masses was verified in 334 patients who underwent cardiac catheterization in our laboratory over 21 consecutive months. A complete two-dimensional echocardiographic (2DE) examination was performed a day before catheterization. The presence or absence of a mass was verified at surgery in 77 patients who successively underwent mitral or aortic valve replacement (51), left ventricular aneurysmectomy with or without myocardial revascularization (25), and resection of atrial myxoma (2). In 32 patients 2DE revealed the presence of a mass-left or right atrial thrombi in 12, left atrial myxoma in 2, left ventricular thrombi in 16, and endocardial vegetations in 2. The other 45 patients were free of intracardiac masses on 2DE. Anatomic verification at surgery revealed the presence of an intracardiac mass in 34 patients. In 30 (true positives) of these, 2DE revealed the mass as well, and in 4 (false negatives) the presence of a mass had not been identified by 2DE. In 2 patients (false positives) the predicted mass was not found at surgery. Absence of a mass was correctly predicted by 2DE in 41 patients (true negatives). Thus 2DE detected intracardiac masses with sensitivity of 88.2% and a specificity of 95.3%. We recommend that 2DE be performed in all patients prior to hemodynamic study and/or cardiac surgery to enable safer management of patients with intracardiac masses during cardiac catheterization and/or cardiac surgery.

Early regression of left ventricular diastolic abnormalities in hypertensive patients treated with nifedipine

SummaryThe effects of nifedipine on blood pressure (BP), left ventricular hypertrophy, and diastolic function were evaluated in 14 patients with essential hypertension (EH). All males with a mean age of 44±6 years (range 35–58 years), and in ten normotensive subjects (control group) aged 32–42 years (mean age 36±4). A complete echocardiogram (ECHO) was performed in basal conditions after 1 and 6 months of therapy with nifedipine (20–40 mg/day). Left ventricular echocardiograms (LV ECHO, M-mode, two-dimensional guided) were plotted with a simultaneous ECG tracing by means of a computerized system that allows evaluation of the following parameters: LV end-diastolic and systolic diameters (EDD, ESD); variations in LV diameter and volume during the entire cardiac cycle, and the velocities of such variations; end-diastolic thicknesses of the interventricular septum and posterior wall (ST, PWT); LV mass, mass/volume (M/V) index, end-diastolic diameter/thickness (D/Th) index, and LV ejection fraction (EF). Left ventricular volume curves were obtained and the contributions of rapid filling (RF) and atrial systole (AS) to EDV were evaluated. Filling velocities during RF (vRF) and AS (vAS) were estimated, as well as the isovolumic relaxation period (IR).No significant changes were observed in the heart rate. After 1 month of therapy, systolic and diastolic BP were significantly decreased (p<0.05). ST and PWT were reduced, with a simultaneous increase in EDD and EDV (p<0.01). LV mass was slightly reduced, as was the M/V index. The D/Th index was increased (p<0.01). The RF contribution to EDV was increased, together with a simultaneous decrease in the AS contribution (p<0.01). The IR period was reduced (p<0.01), while vRF and vAS showed significant increases (p<0.01).After 6 months of therapy, all the above-mentioned modifications were confirmed.In conclusion, mild EH induces early modifications in LV geometry, with consequent LV diastolic abnormalities, characterized by prolonged and incomplete diastolic filling. Thus, LV wall thickness may appear increased, with a simultaneous reduction in LV diameter and volume (without any significant changes in LV mass). Antihypertensive treatment with a Ca2+ antagonist (nifedipine) induces early regression of such abnormalities with normalization of LV diastolic function.

Left ventricular diastolic function and responses to adrenergic stimuli in borderline arterial hypertension

Objective: To detect the existence of a possible relationship between arterial hypertension and adrenergic reactivity to pressure stimuli, and changes in left ventricular diastolic function (LVDF). Patients: Fifty-nine young subjects with borderline arterial hypertension and ten sex- and age-matched controls were investigated. After three medical examinations, the subjects were divided into hypertensive and borderline groups on the basis of the blood pressure reading at visit 3. A complete echocardiographic study was performed in 25 of the 59 subjects. Design: Blood pressure was measured in baseline conditions and during pressure stimuli (mental stress, handgrip and cold pressor tests). LVDF was evaluated primarily by means of filling velocities during diastolic phases taken from the left ventricular volume curve (obtained from a complete echocardiographic study). Results: No significant changes in blood pressure responses were observed for the borderline or hypertensive groups during the adrenergic test. The echocardiographic indices of diastolic function were statistically different for the two groups when compared with the control group. The LVDF parameters correlated significantly with systolic blood pressure and diastolic blood pressure measured at the time of the echocardiogram, but not with blood pressure measured occasionally. Conclusions: Blood pressure increases similarly during adrenergic stimuli in both the hypertensive and borderline groups. The correlation between systolic blood pressure, diastolic blood pressure and LVDF parameters may indicate a very early onset of reduced compliance of the left ventricle, even in a preclinical phase of hypertension.

Direct visualization of aorto-coronary bypass grafts by two-dimensional echocardiography: A new clinical application

An attempt was made to assess noninvasively the patency of aorto-coronary bypass grafts by two-dimensional echocardiography (2-D echo) in 21 patients who underwent myocardial revascularization. Fifteen patients had one graft while the other six had two grafts. All 21 patients underwent angiography 6–18 months after operation. A day before angiography a 2-D echo was performed with the aim of visualizing the bypass grafts. In 18 patients with 23 grafts (13 with 1 graft and 5 with 2 grafts) it was possible to visualize the tract of the graft, by 2-D echo; 16 were judged patent on 2-D echo and confirmed by selective angiography, while 5 grafts were considered occluded both on 2-D echo and angiography. The other 2 grafts were considered to be occluded on 2-D echo but angiographic control displayed their patency. In 3 patients 2-D echo failed to visualize grafts that were patent angiographically. These data must be considered preliminary and need validation in a larger number of patients. However it is reasonable to conclude that 2-D echo has a reliable capacity to predict graft patency. Such an application may be of value in sequential control of patients with aorto-coronary bypass surgery, especially when combined with other clinical and/or technical data.

Modifications in peripheral hemodynamics and left ventricular function in hypertensives treated with nicardipine slow release

Dear Sir, Hemodynamic factors like compliance, characteristic impedance, and peripheral resistance contribute to afterload, an extremely important factor in left ventricular hypertrophy [1,2]. Against this background, we set out to evaluate the action of nicardipine in hypertension [3,4], relating changes in arterial parameters to those in the left ventricular myocardium. We studied 12 male patients (mean age 41 years, range 34-50 years) with mild to moderate essential hypertension, t reated with nicardipine slow release (40 mg twice daily). Peripheral and cardiac hemodynamic parameters were examined basally and after 1 and 6 months treatment. Blood pressure was recorded with a previously validated [5] automatic apparatus (Dinamap 845XT, Critikon, Johnson & Johnson, Tampa, FL). Hemodynamic parameters were recorded using a plethysmographic method for the measurement of pulse wave velocity (variability ± 6%). By means of a Duplex scanner (Diasonics CV 400, Diasonics, Milpitas, CA) with a 10 Mhz probe and a longitudinal power of resolution of 0.3-0.4 mm, we also measured the diameter (variability ± 4%) of the brachial and common carotid arteries, as well as volume flow (variability ± 8%). In the common carotid, diameter was always measured 2 cm from the beginning of the bulbar dilatation, to avoid any mismeasurements. At the same observation times, patients were also subjected to M-mode, two-dimensional echocardiogram and US-Doppler study of transmittal flows. Echocardiograms were analyzed by a previously described computerized system [6]. Means were compared by Students t test for paired data, with allowance for the correction of Bonferroni. Results after 1 month showed a statistically significant reduction in systolic and diastolic blood pressure (147 -3/93 ± 2 vs. 169 ± 7/106 _+ 2 mmHg, mean ± SEM, p < 0.001), which was maintained after 6 months (149 _ 3/94 +__ 2 mmHg, p < 0.001). Over the same period, heart rate showed a slight but never statistically significant increase (first month vs. basal: 69 ± 2 vs. 66 ± 3 beats/min, sixth month: 71 ± 3 beats/min, p ns). The diameter of the brachial (BAD) and common carotid arteries (CCAD), the variations in hemodynamic parameters after 1 and 6 months, and the echocardiographic results are shown in Table 1. Important findings were the improvement of peripheral hemodynamics and also the shift of mass/volume index, show-. ing an increase of the volume in relation to the mass in the left ventricle. Nicardipine SR exerts a significant effect on blood pressure [7], reducing afterload, and on the left ventricular myocardium, improving diastolic compliance and inducing a gradual reduction of hypertrophy. The balanced combination of these actions determines regression of altered left ventricular morphology and function caused by overload, normalizing ventricular performance [8]. In the heart, significant reduction of posterior wall (PWTD) and interventricular septum thickness (IVSTD) was observed, as well as favorable remodeling of the geometry with a significant increase in the end-diastolic transverse diameter of the left ventricle and shortening of its longitudinal diameter, resulting in an increase of end-diastolic volume (EDV). In addition, there was a marked improvement in diastolic function evaluated by the time of isovolumetric relaxation, the percentage contribution of rapid filling (RF/ EDV) and atrial systole to total left ventricular filling (AS/EDV), and the speed of filling (dv/dt) during diastole. When other classes of drugs are used, in the event of actual left ventricular hypertrophy, vascular