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S Ghio

Publications and source records attributed to S Ghio.

At least 37 records · Page 2Linked to original sources
PubMed1993

[The evaluation of intracoronary stents by intravascular echography].

BACKGROUND: Intravascular ultrasound (IVUS) provides high resolution of vessel wall pathoanatomy, and because of the highly reflective nature of stent surfaces, can evaluate alterations in stent geometry. METHODS: This study was performed to assess, by IVUS stent, expansion patterns in patients undergoing implantation of metallic coronary stents, and the mechanisms of restenosis in those patients. Twenty-five patients were studied: 9 pts acutely and 16 pts at routine follow-up 5-8 months after Palmaz-Schatz stent placement. The images recorded by IVUS (25 Mhz 3.9F catheter Intertherapy Inc. California) were quantitatively analyzed for: luminal diameter (LD), luminal cross-sectional area (LA), cross-sectional diameter (SD) and area (SA), comprised by the stent struts. We used quantitative coronary angiography (QCA) (Image Comm System) to measure lumen diameter (LD) and luminal cross-sectional area (LA) in patients in whom IVUS was not performed at the moment of stent placement. These values were considered reference values of LD and LA of the stent at follow-up. RESULTS: During follow-up, patients showed a reduction of vessel lumen LD (2.09 +/- 0.17 mm) measured by IVUS, versus baseline LD (2.87 +/- 0.39 mm) measured by QCA. SD (2.76 +/- 0.31 mm) and SA (6.30 +/- 1.24 mm2) were unchanged in comparison with LD (2.87 +/- 0.39 mm) and LA (6.47 +/- 1.77 mm2) measured by QCA at the time of stent implantation. CONCLUSIONS: These data suggest that the mechanism of restenosis is due to intimal proliferation rather than stent collapse.

Angioplasty, Balloon, Coronary↗
PubMed1993

[The noninvasive quantitative evaluation of the acute hemodynamic effects of sublingual and transdermal nitroglycerin in man].

BACKGROUND: Organic nitrates are complex vasodilators: the hemodynamic action of these drugs is different in the venous and arterial resistance and capacitance beds. The aim of our study was to obtain a quantitative, noninvasive evaluation of the acute effects of sublingual and transdermal (td) nitroglycerin (NTG). METHODS: Twenty-one pts (mean age 49 years) underwent strain-gauge plethysmography and digital photoplethysmography under control conditions, 5 min after sublingual NTG (0.4 mg), 1 hour thereafter and 2 hours after NTG td (10 mg patch). Forearm venous capacitance (CV, ml.100 ml-1) and arteriolar resistance (RA, mmHg.ml-1.100 ml.min) and the b/a ratio of arterial pulse wave (%) were measured. RESULTS: After sublingual NTG, CV increased (+24%, p < 0.01) and b/a was reduced (-35%, p < 0.01), while heart rate and RA increased (+9% and +36% respectively, both p < 0.01). Two hours after NTG td, CV increase was not statistically significant (+11%, p = 0.056), b/a was reduced (-31%, p < 0.01), heart rate and RA did not change. CONCLUSIONS: The combined use of plethysmography and digital photoplethysmography is suitable for the evaluation of vasoactive drugs such as nitrates, which have a complex profile of action on arterial and venous beds. By this method we have shown that NTG td 10 mg dilates venous beds to a low extent; this approach will be utilized in future studies aimed at elucidating dose-response and regimen effect of these drugs.

Administration, Cutaneous↗
PubMed1992

Similar antiischemic effects of intracoronary atenolol and nifedipine during brief coronary occlusions in humans.

To compare the antiischemic effects of intracoronary administration of a beta blocker, atenolol, and of a calcium antagonist, nifedipine, on the clinical and electrocardiographic signs of myocardial ischemia induced by balloon occlusion of the coronary artery, we studied 32 consecutive patients undergoing routine PTCA. In each patient at least three balloon inflations were performed: the first served to verify the occurrence of ischemia (ST segment depression/elevation greater than 1.5 mm); the second was used as a control occlusion; the third was performed after the patients were assigned to receive either atenolol 1.0 mg IC (group 1, N = 16) or nifedipine V = 0.2 mg IC (group 2, N = 16). In a control population of 10 patients, the time to return to baseline of the ECG tended to be progressively shorter during the three consecutive inflations, but the other clinical and ECG parameters did not change significantly. In group 1 and group 2, two patients did not show ECG signs of ischemia at the third inflation; the time to ischemia increased in group 1 (+76%, p less than .001) and group 2 (+85%, p less than .01; NS group 1 versus group 2); ST segment displacement at 30 seconds decreased in group 1 (-38%, p less than .01) and group 2 (-36%, p less than .01; NS group 1 versus group 2).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Different susceptibility to the development of nitroglycerin tolerance in the arterial and venous circulation in humans. Effects of N-acetylcysteine administration.

BACKGROUND: Tolerance to the effects of organic nitrates develops rapidly during continuous exposure to these drugs; its main mechanism seems to be an intracellular sulfhydryl group depletion. However, the relative susceptibility to the development of nitroglycerin tolerance of the arterial or venous circulation in humans is still a matter of dispute. METHODS AND RESULTS: Twenty patients with coronary artery disease underwent a continuous 24-hour nitroglycerin infusion followed by a bolus administration of N-acetylcysteine. Forearm blood flow (ml/100 ml/min) and venous volume (ml/100 ml) were measured by strain gauge plethysmography under control conditions, at the end of nitroglycerin titration, after 24-hour infusion, and after N-acetylcysteine; vascular resistance was calculated as mean cuff blood pressure divided by flow. After 24 hours of nitroglycerin infusion, the initial increase in venous volume was reduced 48% (p less than 0.01), whereas the acute effects on vascular resistance were not attenuated in the whole group. N-Acetylcysteine completely restored nitroglycerin venodilator effects in all 10 patients in whom attenuation of the venous effects was observed during the infusion period. CONCLUSIONS: The data indicate that the susceptibility to the development of nitrate tolerance in humans is higher in the venous than in the arterial circulation, and that the sulfhydryl group donor N-acetylcysteine is extremely effective in reversing nitroglycerin tolerance in the venous circulation in humans.

Acetylcysteine↗
PubMed1992

Clinical evaluation of calcium-antagonist drugs.

Calcium-antagonist drugs are therapeutic agents of first choice in patients with coronary artery disease. We have reviewed a number of clinical trials in which the safety and efficacy of calcium blockers have been tested and discuss the established clinical effects of these compounds, which range from relief of angina and improved quality of life (both in patients with ischemia due to reduction in coronary flow and in patients with ischemia due to increased O2 demand) to a favorable effect on the course of coronary atherosclerosis and, finally, (at least for some of these agents) to an improvement in prognosis.

Angina Pectoris↗
PubMed1991

Granulocyte function in coronary artery disease.

Granulocytes defend the body against invading microbes by producing a complex armamentarium of toxic substances, such as proteolytic enzymes, oxygen radicals and arachidonic acid metabolites. Under certain circumstances, however, such compounds may be released in the absence of phagocytosable particles, resulting in injury to normal cell and connective tissue degradation. Recent experimental studies have emphasized the potential role of granulocytes in the pathogenesis of myocardial ischemia. Clinical investigations have also shown alterations in neutrophil function in stable and unstable clinical manifestations of ischemic heart disease. "Priming" of granulocytes in stable forms of coronary disease may predispose to the subsequent development of acute coronary events, whereas activation of neutrophils may lead to alterations in vascular permeability and coronary flow regulation, leading to further myocardial and endothelial injury in acute myocardial infarction, unstable angina and coronary angioplasty.

Coronary Disease↗
PubMed1991

[Protection against ischemic damage during percutaneous coronary angioplasty].

Minimizing ischemia during percutaneous transluminal coronary angioplasty (PTCA) may lower the risks of the procedure and enhance the short- and long-term success rates of the procedure. However we have to remember that the effects of pharmacological and mechanical interventions during PTCA may be influenced by the functional status of the myocardium. In man the myocardium supplied by a stenotic coronary artery may have a normal metabolic condition or may be stunned, hibernated or even preconditioned by previous ischemic episodes, while the procedure itself may provoke stunning or preconditioning. Many different drugs have been tested for their efficacy under this clinical setting but we recognize that the prolongation of balloon inflation time, though statistically significant, has never proved to be so large to be clinically relevant. Mechanical antegrade coronary infusion (with either blood or oxygenated fluorocarbons) offers the most reliable method for prolonged periods of myocardial protection during PTCA.

Adrenergic beta-Antagonists↗
PubMed1991

[Hemodynamic benefits of sequential atrioventricular pacing].

The purpose of this study was to evaluate the hemodynamic benefits of atrioventricular (A-V) sequential pacing. 30 pts implanted with DDD pacemakers underwent M-mode, B-mode and Doppler echocardiography. In each patient, left ventricular (LV) stroke volume was assessed by measuring the time-velocity integral of mitral inflow in the following modes and rates: VOO at 70 ppm or at the minimum stimulation rate and at 120 ppm; DOO at the same rates with different A-V delay (100, 150, 200, 250 and, whenever possible, 300 msec). The increase in stroke volume obtained with dual chamber pacing at the optimal A-V delay was 45 +/- 25% at 75 ppm and 29 +/- 14% at 120 ppm (p less than 0.05 75 vs 120 ppm). This increase was significantly higher in pts with than in pts without LV hypertrophy (respectively: 51.9 +/- 20.4 vs 36.9 +/- 20.8% at 75 ppm, p less than 0.05 and 33 +/- 13.4 vs 25.4 +/- 14.5% at 120 ppm, p = 0.08). Concerning the A-V delay, we noted that at 75 ppm stroke volume was significantly higher in DOO than in VOO with any A-V delay ranging +/- 100 msec from the optimal one; at 120 ppm the hemodynamic benefit of DOO pacing was observed only when the programmed A-V delay was the optimal one or very near to it. In conclusion, atrio-ventricular sequential pacing allows a significant increase in LV stroke volume over single chamber ventricular pacing both at 75 and 120 ppm. Programming the optimal A-V delay is absolutely necessary to obtain this hemodynamic benefit at the higher stimulation rate.

Aged↗
PubMed1990

Effects of atrial pacing and dipyridamole administration on coronary hemodynamics of collateralized myocardial regions in stable angina pectoris.

Great cardiac vein blood flow by thermodilution and great cardiac vein oxygen saturation were measured in 14 patients with stable exertional angina and an angiographic pattern of complete occlusion of the proximal left anterior descending artery retrogradely filled by collateral vessels supplying still viable myocardium. Measurements were obtained under control conditions, at peak atrial pacing and after dipyridamole administration (0.56 mg/kg intravenously over 4 minutes). Both stress tests induced ischemic electrocardiographic changes in all patients, but dipyridamole administration resulted in greater ST-segment depression in 11 patients (1.6 +/- 0.5 vs 2.4 +/- 1.6 mm, p less than 0.05) and transient ST-segment elevation in 3 patients. Dipyridamole provoked ischemia at a lower value of rate-pressure product (145.3 +/- 30.6 vs 202.9 +/- 36.6 beats/min . mm Hg . 10(-2), p less than 0.0005) and anterior region myocardial oxygen consumption (9.32 +/- 4.76 vs 11.39 +/- 3.91 ml/min, p less than 0.05), despite a greater increase in great cardiac vein flow (139.4 +/- 45 vs 93 +/- 27.4 ml/min, p less than 0.0025) and a greater decrease in the calculated index of anterior region coronary resistance (0.87 +/- 0.27 vs 1.46 +/- 0.43 mm Hg/ml/min, p less than 0.0005). Moreover, great cardiac vein oxygen saturation increased more significantly during dipyridamole-induced ischemia than at peak pacing (63 +/- 12 vs 35 +/- 8%, p less than 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗
PubMed1990

Increased coronary tone in exertional angina: the beneficial effects of calcium antagonists.

Coronary vasoconstriction may play a relevant role in the pathogenesis of exercise-induced myocardial ischemia, not only in patients with Prinzmetal's angina, but also in patients with chronic stable angina. In these patients the use of calcium antagonists, namely, dihydropyridine derivatives, may be beneficial. Hyperventilation is a simple and sensitive test to discriminate patients with effort angina who will improve their exercise capacity after administration of these drugs.

Angina Pectoris↗
PubMed1990

Variable response to atrial pacing after intravenous propranolol in patients with stable exertional angina.

The effect of propranolol administration on regional coronary haemodynamics were investigated in 14 patients with stable exertional angina and isolated left anterior descending artery disease. Thermodilution was used to measure great cardiac vein flow (GCVF) and anterior regional coronary resistance (ARCR) under control conditions, at peak atrial pacing, after i.v. propranolol administration (0.1 mg kg-1) and at the peak of repeated atrial pacing. Propranolol did not change peak pacing heart rate, systolic blood pressure or double product. Peak pacing GCVF decreased slightly but non-significantly after drug administration from 84 +/- 20 to 79 +/- 24 ml min-1, while ARCR increased, but again non-significantly, from 1.36 +/- 0.44 to 1.45 +/- 0.45. Analysis of individual patient responses revealed that propranolol prolonged peak pacing time and hence peak pacing heart rate (from 126 +/- 24 to 140 +/- 23 beats min-1, P less than 0.05) in five patients. In such patients, peak pacing systolic blood pressure was lower than the pre-propranolol atrial pacing (145 +/- 35 vs 165 +/- 33, P less than 0.001) so that double product remained unchanged. Moreover, peak pacing ARCR did not change after propranolol (pre-propranolol 1.47 +/- 0.46, after propranolol 1.40 +/- 0.56 mmHg.ml-1.min, P = ns) while it increased significantly in the nine patients who did not improve after the drug (before propranolol 1.30 +/- 0.44, after propranolol 1.48 +/- 0.41 mmHg.ml-1.min, P less than 0.02). These data suggest that the response to atrial pacing after i.v. propranolol administration is variable as some patients tolerate higher heart rates while others do not.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Increased neutrophil aggregability in coronary artery disease.

The purpose of this investigation was to study neutrophil (PMN) aggregation in the aorta and coronary sinus of 20 patients with angiographically documented coronary artery disease (group I) compared with eight patients with normal coronary arteries (group II). PMNs were separated from the other blood components and their aggregation response to Ca2+ ionophore A 23187 l x 10(-5) M (final concentration) was measured. Group I patients had higher aggregating activity in the coronary sinus than in the aorta (24.9 +/- 3.7 vs 18.7 +/- 3.4 average maximum delta T, P less than 0.01), while no difference was found in group II (coronary sinus 16.7 +/- 3.5; aorta 16.3 +/- 2.4 average maximum delta T P = NS). Among group I patients, smokers had a significantly higher aggregating activity than non-smokers, whereas no correlation was found between aggregation response and blood cholesterol values. These data suggest that the presence of atherosclerotic plaques in coronary vessels may prime PMNs so that they show greater aggregating response to subsequent stimulation.

Aorta↗
PubMed1989

Long-term survival and risk stratification in patients with angina at rest undergoing medical treatment.

In order to determine those factors which influence long-term prognosis in patients with angina at rest associated with transient ST-segment changes, 217 patients undergoing medical treatment were followed for a mean of 39 months. All patients underwent coronary arteriography. Univariate analysis identified 12 variables significantly related to prognosis. These were disease of the left main coronary artery; the number of diseased vessels; left ventricular end-diastolic pressure; ejection fraction; baseline electrocardiogram; presence of prior myocardial infarction; ST-segment depression and ventricular arrhythmias during pain; disease of the proximal anterior descending coronary artery; crescendo angina; hypertension; and age. Use of the Cox regression model for survival analysis revealed only 3 variables which were independent predictors of prognosis. They were disease of the left main coronary artery; the number of diseased vessels and left ventricular end-diastolic pressure. The model allowed stratification of patients into 3 groups. Survival at 3 years was 98% in the low risk group; 82% in the intermediate risk group; and 58% in the high risk group. These data indicate that disease of the left main coronary artery, the number of diseased vessels and left ventricular end-diastolic pressure are the independent predictors of prognosis in angina at rest. These variables may allow stratification of patients into groups having different long-term survivals.

Adult↗
PubMed1988

Acute haemodynamic effects of diltiazem in patients with recent Q-wave myocardial infarction.

The effects of diltiazem on left ventricular systolic and diastolic function were studied in 14 patients with a recent (12-20 days) Q-wave myocardial infarction. Left ventriculography with simultaneous recording of high-fidelity left ventricular pressure was performed in control conditions, and after i.v. administration of diltiazem (0.2 mg kg-1 as a bolus followed by constant infusion of 0.005 mg kg-1 min-1 lasting 8-10 min). After the administration of the drug, left ventricular systolic pressure decreased by 12.7% and mean circumferential wall stress by 14% (both P less than 0.01); the heart rate did not change; the ejection fraction increased by 9.6% (P less than 0.05) and maximum dP/dt/P by 11% (P less than 0.01). Quantitative segmental wall motion analysis showed that the beneficial effects of diltiazem on global left ventricular systolic function were associated with an increase in contraction in hypokinetic regions, where they were supplied by normal or diseased coronary vessels (both P less than 0.01). Left ventricular end-diastolic pressure decreased by 23.6% (P less than 0.05) and minimal diastolic pressure by 38% (P less than 0.05). Passive diastolic properties of the left ventricular chamber remained unaltered but isovolumic relaxation markedly improved: the T constant decreased 26% (P less than 0.01). Thus, in patients with a recent Q-wave myocardial infarction, the i.v. administration of diltiazem unloads the left ventricular chamber without showing depressant effects on myocardial contractility.

Adult↗