Biomedical subjects
Publications and source records attributed to I Sheiban.
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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.
The beneficial effects of calcium-channel blockers against myocardial stunning have been tested in experimental studies, showing that, when added before or during ischemia, a protective effect against postischemia stunning is achieved. The present study was undertaken to test and compare the protective effect of calcium antagonists [nisoldipine (NIS) and nifedipine (NIF)] and nitrates (NIT) against myocardial stunning in patients with coronary artery disease undergoing percutaneous transluminal coronary angioplasty (PTCA) with prolonged inflation as PTCA represents a model of induced acute and severe ischemia for a brief period and might cause myocardial stunning. The study included 30 patients between the ages of 42 and 67 years, all with exercise-induced angina and single-vessel disease, with severe stenosis (80% to subtotal occlusion) localized on the left anterior descending artery and with the absence of collaterals on the coronary angiograms. Moreover, all patients had normal left ventricular (LV) overall function, as well as normal systolic thickening of the anterior wall, supplied by the diseased artery. Patients were randomized to a pre-PTCA treatment with NIT, 80-120 mg/day (10 patients), NIF, 40-60 mg/day (10 patients), and NIS, 10-20 mg/day (10 patients). Pre-PTCA treatment was initiated 7 days before the procedure and continued after. During the PTCA, at the first balloon inflation, an additional dose of 300 micrograms of NIT was injected into the left anterior descending artery through the balloon catheter in the patients in the NIT group, as well as 0.2 mg of NIF in NIF group patients and 0.05 mg of NIS in NIS group patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of nifedipine SR and lacidipine on blood pressure, left ventricular (LV) hypertrophy, and diastolic function were evaluated in 15 male patients (mean age of 45 +/- 8 years) with mild-to-moderate hypertension. Clinical evaluation and complete echocardiography were performed at baseline (after 15 days of washout). Seven patients received nifedipine SR (20-40 mg twice daily) and eight lacidipine (4-6 mg once daily). Clinical evaluation and complete echocardiography studies were repeated after 1 and 6 months of active treatment. In addition, full echocardiographic evaluations were carried out in 10 normotensive subjects (for comparison). Results were similar with either drug. After 1 month of therapy, systolic and diastolic blood pressures were significantly decreased (p less than 0.05); after 6 months of therapy, further changes were observed, confirming their significance. Analysis of our data suggests that (a) mild essential hypertension induces early modifications of LV geometry with consequent LV diastolic function characterized by a prolonged and incomplete diastolic filling; thus, LV wall thickness may be increased with a simultaneous reduction in LV end-diastolic short-axis diameter and volume; and (b) antihypertensive treatment with calcium antagonists such as nifedipine SR and lacidipine leads to early normalization of LV geometry and diastolic function without a significant change in total LV mass.
Myocardial stunning might be defined as a transient postischaemic contractile abnormality seen after reperfusion has been achieved. The benefits of reperfusion therapy might be delayed, but will occur within hours to days after reperfusion. Consequently, the stunned myocardium is viable, but its full recovery might be delayed for a few weeks. While multiple pathophysiological mechanisms are reported to be responsible for the stunning phenomenon, a partial failure of calcium cycling seems to be the cause of the electromechanical uncoupling demonstrated in the stunned myocardium. No pharmacological or other means were used to detect myocardial viability in the stunned myocardium since it is, by definition, a viable myocardium. The 'hibernating' myocardium differs from the stunned myocardium in that it is a viable (partially or completely), chronically underperfused myocardium with an impaired metabolism and function which is slowly reversible when adequate blood flow is restored. This condition represents an 'extreme defence mechanism' in response to profound and chronic ischaemia; however, it does not occur in all patients with chronic myocardial ischaemia. In some circumstances the myocardium might undergo ischaemic necrosis instead of hibernation, with irreversible structural and functional damage. The mechanism leading to one or other response to chronic ischaemia is unclear and might depend on the degree and duration of myocardial ischaemia and histopathological response. Thus, the detection of hibernated myocardium is highly significant because it constitutes a potentially salvageable myocardium. The gold standard for the clinical detection of these conditions is positron emission tomography (PET), but it is uncertain what role echocardiography and pharmacological tests could play in this field.
The 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 less than 0.05). ST and PWT were reduced, with a simultaneous increase in EDD and EDV (p less than 0.01). LV mass was slightly reduced, as was the M/V index. The D/Th index was increased (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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.
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.
The effects of two antihypertensive agents, nifedipine (N) and captopril (C), on left ventricular (LV) mass and volume were studied in 16 patients with essential hypertension (8 treated with N and 8 with C for 6 months) by means of a complete M-mode echocardiogram monitored by two-dimensional echocardiography. Both N and C induced a significant reduction in end-diastolic, but not systolic, posterior wall and septum thickness and an increase in end-diastolic volume, but not in end-systolic volume. A significant increase in the contribution of rapid filling together with a simultaneous reduction in the contribution of atrial systole to end diastolic volume were also observed. The reduction in LV wall thickness and mass after both C and N might be attributed to an improvement in diastolic function and to a reduction in wall tension, rather than to an effective regression of LV hypertrophy.
Platelet glutathione peroxidase (GSH-Px) activity was measured in 25 healthy individuals and in 25 patients affected with well-documented coronary artery stenosis. In parallel, malondialdehyde (MDA) production was assayed on platelets following stimulation with sodium arachidonate. Mean platelet GSH-Px activity was significantly reduced and mean platelet MDA production was significantly increased in the patient group. The difference observed in the GSH-Px activity might be a consequence of different nutritional habits, suggesting an impaired intake of selenium, the inorganic moiety of GSH-Px. As low GSH-Px activities in human platelets may be associated with increased MDA and thromboxane production, we hypothesize that a low enzyme activity may be a risk factor for the development of coronary artery disease.
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Mechanical complications of prosthetic valves are increasing. The following report describes a case of fracture of a Björk-Shiley mitral prosthetic strut with dislogment of the valve occluder into the thoracic aorta. At the reoperation a new prosthesis was implanted but the patient died of acute heart failure. The diagnosis of valve disfunction must be made non invasively, because the time required for cardiac catherization usually constitutes a lethal delay. The only hope for survival is prompt surgical treatment.
The ability of ECG-VCG to predict the severity of postinfarction LV asynergy was evaluated in 152 patients with previous myocardial infarction who underwent left cineventriculography in the right anterior oblique view. Various ECG and VCG signs were examined in order to predict the existence of severe asynergy in general (dyskinesia or akinesia or severe hypokinesia) and of dyskinesia in particular. In patients with inferior myocardial infarction (Group A) persistent ST segment elevation was the only specific ECG sign (100%) of severe asynergy; it had a poor sensitivity (6.2%). Four frontal VCG signs (presence of terminal bite, y- greater than 0.18 mV, maximum early superior vector along x axis = MESV greater than or equal to 1.3 mV, duration of initial superior forces = DISF greater than 50 msec) increased the sensitivity of the ECG-VCG method to 75.8% while maintaining a 100% specificity. Regarding the diagnosis of dyskinesia, only the ECG sign of persistent ST segment elevation and the VCG sign of y- greater than or equal to 0.3 mV had a 100% specificity. The sensitivity of the ECG-VCG method was 33.3% (16.6% ECG and 16.6% VCG). In patients with anterior myocardial infarction (Group B), concerning the diagnosis of severe asynergy, the ECG signs of sigma ST greater than 3 mm in anterior leads; pathologic Q wave in four or more anterior leads (including D1 and aVL); and the presence of LAH or LAH + RBBB, had a 100% specificity and a good sensitivity (60.5%). The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 71% while maintaining a 100% specificity. As for the diagnosis of dyskinesia, the ECG signs with a 100% specificity were sigma ST greater than or equal to 5 mm in anterior leads, a pathologic Q wave in more than five anterior leads (including I and a VL) and RBBB + LAH; these variables had a sensitivity of 48.3%. The VCG sign of a narrow horizontal QRS loop increased the sensitivity of the ECG-VCG method to 79.3% while maintaining a 100% specificity. In patients with inferior plus anterior myocardial infarction (Group A + B) the signs mentioned above for each group were evaluated, confirming a 100% specificity. Regarding the diagnosis of severe asynergy, the ECG signs had a sensitivity of 61.3%, while VCG increased the sensitivity of the ECG-VCG method to 90.3%.(ABSTRACT TRUNCATED AT 400 WORDS)
The anti-anginal effect of oral verapamil was assessed in 12 patients with chronic effort-induced angina, using a single-blind, placebo-controlled protocol. The patients were given, in random order, placebo, verapamil 240 mg/day, verapamil 360 mg/day, for 24 hours, followed by a 24-hour washout period. Increase in tolerated work load, compared to a baseline bicycle exercise test, was -25 +/- 55.9 kgm/min on placebo, 137.5 +/- 96 on verapamil 240 mg/day, 212.5 +/- 129.3 on verapamil 360 mg/day (p less than 0.001). While taking verapamil in 9 patients 240 mg/day the test was interrupted with of ECG alterations; at the same work load, only 1 patient had ECG alterations while taking verapamil 360 mg/day (p less than 0.01) and 9 completed the test without ECG alterations. The pressure-rate product at maximum exercise was not significantly affected by treatments. The higher dosage of verapamil prolonged the P-R interval (p less than 0.01) but only 1 patient had first-degree AV block. It is concluded that verapamil is a powerful and safe drug in the treatment of effort-induced angina: there is evidence that the effect depends on the dosage administered.
Between May 1978 and July 1981 at the Department of Cardiovascular Surgery, Padua University Medical School in Verona, 10 patients with coarctation of the aorta underwent surgical treatment with a by-pass between the left subclavian artery and the descending aorta. A synthetic fibre graft was employed. The patient's age varied between 20 and 46 years and all were hypertensive: 160-220 mmHg systolic, 90-110 diastolic pressure. No hospital deaths occurred. Blood pressure decreased significantly in all patients as well as their electrocardiographic signs of left ventricular hypertrophy.
Change in R wave amplitude (mean delta R) was measured sequentially during and after 12 lead maximal treadmill exercise tests in 14 subjects with normal coronary arteries and 62 patients with coronary artery disease. In normal subjects mean delta R decreased maximally one minute after exercise and returned to control levels within three minutes. In contrast, mean delta R increased in patients with coronary artery disease, the greatest change occurring in patients with either triple vessel or left main disease or those with an akinetic region on the left ventriculogram. R wave amplitude returned to resting levels in five minutes. Increase in R wave amplitude was not directly related to changes in the ST segment. Changes in R wave amplitude during maximal treadmill exercise may improve the discrimination between patients with and without coronary artery disease and may help to identify those patients with abnormal left ventricular function.
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