Localization of mitral periprosthetic leaks by transesophageal echocardiography.
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Biomedical subjects
Publications and source records attributed to A Cherchi.
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The aim of this study was to investigate the anti-ischemic and antianginal activity and the duration of the new dihydropyridine calcium blocker nisoldipine (NIS) in patients with stable angina pectoris. The research was carried out on 16 patients, all male, 41-68 (mean of 58) years of age, with stable angina pectoris and fixed ischemic threshold (variations < 15%). After a 10-day washout period, patients were randomized to treatment with either 10 mg of nisoldipine or placebo (PL), twice daily for 21 days, according to a double-blind, crossover design. Patients underwent maximal symptom-limited exercise testing at 10 W/min on a bicycle ergometer, twice during the washout period, and once at the end of each treatment period, 3 and 12 h after oral administration of the drugs. In comparison with placebo, nisoldipine increased the ischemic threshold (N, 704 +/- 45 s; PL, 548 +/- 35 s; p < 0.01) and anginal threshold (N, 766 +/- 44 s; PL, 699 +/- 42 s; p < 0.01) for at least 12 h, and the ST-segment depression significantly decreased at maximal work (PL, 2.4 +/- 0.1 mm; N, 1.8 +/- 0.2 mm; p < 0.01) and at maximal common work (PL, 2.4 +/- 0.1 mm; N, 1.15 +/- 0.2 mm; p < 0.01). Similar to placebo the rate-pressure product was not significantly changed at higher submaximal effort after N, but it was significantly increased at the level of ischemic threshold, suggesting an increase in coronary blood flow to ischemic zones. Nisoldipine possesses anti-ischemic and antianginal activity lasting at least 12 h. This activity seems to be due to an increase in coronary blood flow to ischemic zones.
Gallopamil (GSR) is a new calcium-channel blocker. The anti-ischemic activity of GSR was investigated in 12 patients with stable angina of effort, with fixed ischemic threshold (variations < 15%). After a 7-day washout period, patients were randomized to receive treatment with either GSR 100 mg or placebo twice daily for 7 days. Patients underwent maximal symptom-limited exercise test, 10 W/min on a bicycle, during washout (twice) and after the end of each treatment period. Patients were studied by electrocardiogram and the cuff method for determining systolic blood pressure. After treatment with GSR, ischemic and anginal thresholds were increased for at least 12 h in comparison with placebo (ischemic threshold: GSR 663 +/- 37, placebo 571 +/- 36, p < 0.01; anginal threshold: GSR 708 +/- 32, placebo 646 +/- 38, p < 0.05). Rate-pressure product was not changed at the same levels of exercise, but it was significantly increased during exercise at ischemic threshold. In conclusion, GSR possesses an anti-ischemic and antianginal activity lasting at least 12 h. This activity seems due to an increase of coronary blood flow to ischemic areas.
The aim of this research was to assess whether the antihypertensive therapy with nifedipine, a dihydropyridine calcium-antagonist, is able to control hypertension not only at rest but also during exercise. So, 20 male hypertensive patients, mean age 48 years, were evaluated by symptom limited bicycle exercise (10 W/min) before and after 6 and 12 months of therapy with nifedipine in a slow releasing form (40-60 mg/day). Exercise tolerance significantly increased after 12 months of antihypertensive therapy with nifedipine (from 146 +/- 5 to 153 +/- 4 W, p < 0.05). Systolic and diastolic blood pressure decreased after 6 and 12 months both at rest (from 160 +/- 6/109 +/- 9 mmHg to 132 +/- 3/91 +/- 3 and 135 +/- 4/93 +/- 1 mmHg, respectively, both p < 0.001) and during exercise (at end exercise: from 238 +/- 7/121 +/- 5 mmHg to 216 +/- 6/106 +/- 3 and 213 +/- 6/107 +/- 3 mmHg, respectively, both p < 0.001). No significant changes in heart rate were observed during antihypertensive therapy both at rest and during exercise test. In conclusion, long-term antihypertensive therapy with nifedipine was effective in the control of hypertension both at rest and during physical stress. Moreover, an improvement in effort tolerance was observed in hypertensive patients.
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To evaluate the influence of antihypertensive therapy (AHT) on blood pressure (BP) seasonal variations, we have analyzed the systolic and diastolic BP values in 145 hypertensives, 112 males and 33 females, aged 23-65 years, in the 10-year period 1981-1990. All patients received medical treatment and were examined for at least 5-7 consecutive years. The year was divided in 2 (cold and warm months) and 4 periods in relation to mean monthly environmental temperature (10 degrees C, 13 degrees C, 18 degrees C and 23 degrees C). Systolic and diastolic BP was higher in cold months (142/93 vs 137/88 mmHg, p less than 0.05). In cold periods AHT was increased in 11% of patients and decreased in 8%. In the warm periods AHT was decreased in 11% of patients and increased in 6%. The AHT reduction in the warm months was not significantly different in comparison to that of cold months. Vice versa, the AHT increase in cold months was greater than that of warm periods (p less than 0.001). In the 10-year period considered, 18% of patients reduced AHT in the warm period and increased it in the cold period. It was also found a small correlation between diastolic blood pressure and wind, which is, in our country, mostly the mistral. Betablockers, calcium-antagonists and the association betablocker-diuretics showed a seasonal BP variation, while patients treated by diuretic had the same BP both in winter and in summer. A small negative correlation was observed between systolic and diastolic BP and temperature in patients treated by all antihypertensive drugs except the diuretics.(ABSTRACT TRUNCATED AT 250 WORDS)
The influence of cardioselectivity and/or intrinsic sympathomimetic activity (ISA) of betablockers on hemodynamic antihypertensive effect and on left ventricular (LV) dimensions and function was studied by echocardiography in 72 hypertensive patients, mean age 43 years. After 15 days of placebo, active therapy was given for 1 month: acebutolol (ACEB, n: 16, 400-800 mg/day), atenolol (ATEN, n: 16, 50-100 mg/day), pindolol (PIND, n: 13, 15-30 mg/day), timolol (TIMO, n: 15, 10-20 mg/day) and nadolol (NADO, n: 12, 80-160 mg/day). All betablockers showed effective antihypertensive activity. Betablockers without ISA (ATEN, TIMO, NADO) reduced cardiac output (p less than 0.05), those with ISA (ACEB, PIND) decreased total peripheral resistance (p less than 0.01 and p less than 0.05 respectively). Independently from ISA, cardioselective betablockers (ATEN, ACEB) increased LV end diastolic dimension and stroke volume (p less than 0.05). LV mass was not changed, although interventricular septum thickness decreased after TIMO and NADO (p less than 0.05). LV function, as assessed by fractional shortening, was not impaired by any betablocker.
The aim of this study was to evaluate the anti-ischemic efficacy of 2 different doses of benazepril (B), a new ACE-inhibitor, 10 and 20 mg, given per os. Fifteen male patients gave informed, written consent; they were aged 40-67 years, with stable effort angina pectoris and were randomly given, in double-blind condition, a tablet containing B 10 mg, B 20 mg or placebo (PL), once a day, according to a 3 x 3 latin square design. Bicycle exercise tests were performed on the same day, 2 and 10 hours after the last drug intake. B 10 mg and B 20 mg, in patients with stable effort angina, compared to placebo, increased ischemic threshold and decreased ischemic ST depression at maximal work, after 2 hours but not after 10 hours. In conclusion B 10 mg and B 20 mg showed anti-ischemic activity 2 hours after drug intake.
To assess the behaviour of blood pressure (BP) during exercise in hypertensive patients (H), 103 males aged 21 to 59 years (mean 43 years) with essential hypertension WHO class I-II were studied. All H, without antihypertensive therapy for at least 15 days, underwent sitting bicycle exercise (10 W/min). BP was measured on the left arm by a standard mercury sphygmomanometer. The fifth Korotkoff phase was taken as the diastolic pressure. Heart rate was measured by electrocardiogram. Subjects were studied at rest in sitting position, during exercise every 3 min and during recovery at 1, 3 and 5 min. As controls we took 100 normotensive (N) males aged 20 to 59 years (mean 39 years). The results were analyzed also by decades. Systolic (S) and diastolic (D) blood pressure were higher in H in comparison with N at rest, in sitting position, (N 119 +/- 10/79 +/- 7 mmHg; H 162 +/- 21/112 +/- 11 mmHg; p less than 0.01), during exercise and recovery. SBP and, to a lesser extent DBP, progressively increased during exercise both in N and in H patients (at peak exercise: N 192 +/- 20/85 +/- 13 mmHg; H 239 +/- 25/121 +/- 13 mmHg, p less than 0.01). The mean increase of SBP during exercise was 77 mmHg in H and 73 mmHg in N (NS). DBP increment was about 6 mmHg in N and 9 mmHg in H (NS). Within the age decades, SBP during exercise was higher in the age group of 50 to 59 in comparison with 20 to 29 in N and H (p less than 0.05) and DBP in the age group of 40 to 49 and 50 to 59 in comparison with 20 to 29 and 30 to 39 (p less than 0.01). The fall of SBP and DBP was greater at 1 min of recovery both in H and N and became progressively smaller thereafter. At a same workload (90 and 120 W) 60% of H had SBP and 85% had DBP higher than BP in N (above 200/104 mmHg--mean + 2 SD--at 90 W and 215/106 mmHg at 120 W). No difference was observed in heart rate at rest and during exercise between N and H. In conclusion, H had SBP and DBP higher at rest, during exercise and recovery in comparison with N. However, a parallel increase of BP was found in the 2 groups during exercise. Ergometric test showed that 60-85% of H had also excessive increase of systolic and diastolic blood pressure during exercise.
The aim of this study was to investigate antianginal and antiischemic activity and tolerance of a new nitrate derivative, nicorandil (N). This research has been carried out in 18 patients, aged 47-70 years, suffering from stable effort angina with fixed ischemic threshold. The study started with 10 days of washout, during which the patients exercised twice on bicycle to verify the reproducibility of the test. Then, they took N or isosorbide-5-mononitrate (ISM) for 14 days according to a double blinded cross-over balanced study. Between the 2 periods patients took placebo (PL) for 14 days. In the first day and in the last day of each period, 2 hours after the last drug intake, patients performed a stress test on bicycle. Like ISM, N significantly increased, versus PL, 1 mm of ST depression time (ischemic threshold) in the first and in the last day, without differences between the 2 drugs and between the days. Moreover, ST depression was significantly lower at maximal common work (MCW) versus PL. The rate-pressure product was not different from PL after N and ISM at maximal common work, but is was increased at the ischemic threshold. In conclusion, like ISM, N has shown antiischemic activity in patients suffering from stable angina pectoris on effort with fixed ischemic threshold. After 14 days of treatment there was no evidence of tolerance. The activity of N seems essentially due to an increase of coronary blood flow to ischemic zones.
Atherosclerosis is a degenerative disease responsible for the majority of deaths in the western populations. According to the idea of the reaction to injury the endothelial cells lining the vascular wall are exposed to repeated insults to their integrity. The injury results in a loss of functional attributes of endothelium and leads to a sequence of events including platelet adherence and aggregation, release of platelet granular components, migration and proliferation of medial smooth muscle cells into the intima. Examples of types of injury include chemical injury, as in hyperlipidemia, or mechanical stress associated with critical changes in vascular flow. Atherosclerosis has been considered a disease primarily concerned with lipid metabolism by regarding the intramural caseous material of atheromatous arteries as the sine qua non of the disease. The limitation of the lipid theory is that the conventional cholesterol-fed animal does not exactly reproduces the pathology of atherosclerosis. An alternative theory suggests that atherosclerosis is induced by mechanical fatigue which produces the progressive change in structure and mechanical properties of the vessel wall. In this view the lipid accumulation is a secondary phenomenon, the consequence of concomitant biochemical alterations of mural constituents. The hypothesis of reaction to injury provides a plausible explanation for the lesion formation and the different theories of atherogenesis are not mutually exclusive.
Clinical trials, during myocardial infarction, showed the importance of thrombolytic therapy on coronary patency, to improve left ventricular function, to reduce early and late mortality. Since the efficacy of thrombolytic therapy is now well established, most clinical trials were made to compare the efficacy of SK, rt-PA and APSAC and to evaluate concomitant drugs. Recanalization and coronary patency, reocclusion and incidence of side effects, left ventricle function's improvement and lowered mortality have been used to assess drugs' activity. At the moment the efficacy of three thrombolytic drugs seems to be the same. So the drug's choice is related not to drug's efficacy but to side effects of the drugs. Concomitant intravenous heparin therapy is now under study; utility of this therapy is shown by its theoretical assumptions and by clinical trials results. Large clinical trials are working to extend our knowledge, improving the patients' management in our every day clinical practice. Furthermore, large trials do not replace but go together with studies performed on few patients, whose results often give advance notice of those of large ones.
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