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Biomedical subjects

S Caponnetto

Publications and source records attributed to S Caponnetto.

At least 19 recordsLinked to original sources
PubMed1996

Insulin-like growth factor-I and angiographically documented coronary artery disease.

In conclusion, we have reported an association between low IGF-I concentrations and CAD in relatively young men. This observation raises the possibility that IGF-I deficiency could be part of the polymetabolic syndrome. Whether a subnormal IGF-I production is due to growth hormone secretory abnormalities or to other metabolic reasons (e.g., insulin resistance or fat distribution, or both) is still unknown.

Adult↗
PubMed1996

Cerebral blood flow reserve in patients with syndrome X.

BACKGROUND: Patients with syndrome X frequently show disorders of oesophageal motility, bronchial reactivity or impaired vasodilator capacity of peripheral vascular beds. For these reasons, it has been suggested that syndrome X may represent a generalized abnormality of vascular and non-vascular smooth muscle function, rather than an isolated coronary problem. OBJECTIVE: To measure the cerebral blood flow and cerebrovascular vasodilator reserve in syndrome X patients and in controls. METHODS: We measured the cerebral blood flow and cerebrovascular reserve in 16 patients with syndrome X [11 women, aged 59.5 +/- 10.8 years (mean +/- SD)] and in 16 age-matched healthy volunteers. No patients had evidence of stenoses of carotid and vertebral arteries on Doppler sonography. Cerebral blood flow was measured by the 133Xe inhalation method, using the initial slope index as the cerebral blood flow index. After a baseline measurement, a second cerebral blood flow measurement was performed 20 min after administration of 10 mg/kg acetazolamide intravenously. Acetazolamide is known to be a potent cerebral vasodilator. The percentage increase in cerebral blood flow after acetazolamide administration was considered an index of cerebrovascular vasodilator reserve. RESULTS: Under basal conditions, both regional and global cerebral blood flow were nearly identical in the control group and in the patient group (initial slope index 50.2 +/- 3.8 versus 50.3 +/-6.2, NS). After acetazolamide administration, the cerebral blood flow increase was 29.0 +/- 14% in the patient group and 29.5 +/- 11% in the control group (NS). CONCLUSIONS: Our data show that cerebral blood flow and cerebrovascular vasodilator reserve were preserved in a series of patients with syndrome X. These results are not consistent with the hypothesis of a diffuse smooth muscle disorder.

Acetazolamide↗
PubMed1996

Recognition and treatment of unstable angina.

Despite the growing number of patients discharged from hospital with a diagnosis of unstable angina, the diagnostic procedures and treatment of unstable angina are still greatly debated, as they have been for patients with myocardial infarction. In recent years the definition and classification of the clinical syndrome of unstable angina has been subjected to numerous proposals by distinguished cardiologists. An attempt to clarify and redefine practical guidelines for different subgroups of patients has been developed and carried out by the US Agency for Health Care Policy and Research (AHCPR). The current medical approach to treatment of patients with unstable angina is discussed in detail, analysing the role of antiplatelet medications, beta-blockers, nitrates, heparin and calcium antagonists. The small subgroup of patients with refractory unstable angina should undergo urgent coronary angiography and revascularisation. Previous and current research on medical treatment with thrombolytic therapy, GPIIb/IIIa platelet receptor blockers and direct thrombin inhibitors is outlined, keeping in mind one of the main aspects of pathophysiology of the disease, that is ongoing thrombus formation. In the future, a more aggressive strategy aimed at normalising the atherogenic lipid profile in this very high risk group of patients should be carried out, based on the positive results of lipid-lowering drug trials both in primary and secondary prevention.

Adrenergic beta-Antagonists↗
PubMed1995

Perfusional and metabolic effects of nisoldipine as shown by positron emission tomography after acute myocardial infarction.

After myocardial infarction, regional dysfunction can occur in viable myocardial regions because of the presence of baseline hypoperfusion. Recent evidence suggests that these areas may maintain a residual perfusion reserve. The aim of the present study was to evaluate whether oral nisoldipine can increase regional myocardial blood flow (MBF) in dyssynergic but viable myocardium after myocardial infarction. Patients with isolated left anterior descending coronary stenosis were studied 1 month after the first myocardial infarction. Patients underwent [18F]fluorodeoxyglucose imaging, and MBF was measured, using positron emission tomography and [13N]ammonia, at baseline and following dobutamine administration (10 micrograms/kg/min over 5 minutes). MBF measurements were repeated 24 hours after nisoldipine (10 mg twice daily). Preliminary results suggest that necrotic areas showed the largest reduction in baseline MBF. Dyssynergic-viable regions showed a reduced resting MBF but maintained a residual perfusion reserve in response to inotropic stimulation. Thus, nisoldipine selectively improved basal perfusion in dyssynergic-viable myocardium.

Adult↗
PubMed1995

Lipoprotein (a) is increased in acute coronary syndromes (unstable angina pectoris and myocardial infarction), but it is not predictive of the severity of coronary lesions.

Lipoprotein (a) [Lp(a)] concentrations were determined in 365 patients undergoing coronary angiography for stable angina (n = 159), unstable angina (n = 99), recent myocardial infarction (n = 45), and nonischemic heart disease (cardiomyopathy or valvular disease, n = 62, non-IHD). Mean +/- SD and median Lp(a) concentrations in stable angina (29.9 +/- 29.2;22 mg/dl) did not differ from those in non-IHD (26.9 +/- 26.3; 17), but were significantly lower than in patients with unstable angina (52.7 +/- 36.6; 58) and myocardial infarction (44.8 +/- 36.4; 34) (p < 0.01). Coronary angiography revealed that 261 patients, including 4 patients in the non-IHD group, had significant (> or = 50%) coronary lesions. Lp(a) was higher in patients with (41 +/- 35; 32) than in those without (28 +/- 27; 19) angiographic evidence of significant coronary stenosis (p < 0.05) and showed a weak univariate correlation with the angiographic index (Total Score) of the severity of the disease (r = 0.106;p < 0.05). However, in the subgroup of 303 patients with stable/unstable angina or myocardial infarction, Lp(a) was predictive neither of angiographic presence nor of severity of coronary disease. Patients were then ranked according to the Total Score values. Among patients with comparable angiographic severity of coronary artery disease, Lp(a) appeared to be remarkably higher in patients with acute ischemic syndromes (unstable angina, myocardial infarction) than in patients with stable angina. In conclusion, Lp(a) was roughly twice as high in acute (unstable angina, myocardial infarction) than in chronic (stable angina) ischemic syndromes, but there was no difference between chronic stable angina and non-IHD.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina, Unstable↗
PubMed1995

Right ventricular dysplasia as a generalized cardiomyopathy? findings on magnetic resonance imaging.

The aim of our study was to define cardiac morphological and functional abnormalities of right ventricular dysplasia by magnetic resonance imaging. Twenty-two healthy volunteers (age, 37.7 +/- 14.2 years) free of cardiac or respiratory diseases (group I) and 12 patients (age, 41.9 +/- 15.8 years) with clinical, electrophysiological and cineangiographic diagnosis of right ventricular dysplasia (group II) underwent magnetic resonance imaging at 0.2 Tesla. End-diastolic diameter, trabecular disarray and segmental wall motion abnormalities were evaluated for the right ventricle as were adipose replacement and fractional shortening for both ventricles. The right ventricular end-diastolic diameter was significantly enlarged in group II (P = 0.0023). Right ventricular trabecular disarray was mild in two group I subjects, and moderate in seven and massive in five group II patients. Right ventricular systolic bulges were found in seven group II patients, aneurysms in five. Excellent agreement was found between magnetic resonance imaging and cineangiography for bulges, aneurysms and tricuspid regurgitation (P < 0.0001). On spin-echo images, signal hyperintensities, due to adipose replacement, were found in 44 cardiac regions in group II: right ventricular outflow tract (12), sub-tricuspid posterobasal region (8), right ventricular apex (9), right ventricular anterior wall (6), interventricular septum (4), left ventricular lateral wall (4), left ventricular apex (1). Significant signal-to-noise ratio differences were found between group II abnormal areas and group I myocardial tissue for the right (P < 0.0001) and left ventricles (P = 0.0006). Fractional shortening in the right and left ventricles were significantly reduced in group II (P = 0.0002 and P = 0.00016, respectively). Magnetic resonance imaging can be considered a very useful diagnostic tool for the detection of features typical of right ventricular dysplesia, such as adipose replacement, trabecular disarray, bulges and aneurysms and provides useful information about cardiac function and regional wall motion. It indicates that left ventricular involvement occurs in a significant fraction of patients, and suggests that right ventricular dysplasia may be a generalized cardiomyopathy.

Adolescent↗
PubMed1994

Efficacy of L-propionylcarnitine treatment in patients with left ventricular dysfunction.

The effect of L-propionylcarnitine on patients with left ventricular dysfunction (EF < 45%) NYHA class II, symptomatic despite therapy with digitalis and diuretics was evaluated in a phase II parallel, double-blind, randomized, placebo-controlled study. Fifty patients (28 men and 22 women) aged 37-70 years received 1.5 g of L-propionylcarnitine or placebo on a random basis as oral treatment for 6 months. At baseline, during a 7 day placebo run-in period, and during the 6-month treatment bicycle exercise test, M-B mode and Doppler echocardiography, and clinical evaluation (clinical score) were repeatedly performed. The analysis of variance for repeated measurements showed a statistically significant difference (P < 0.01) in the mean value of exercise time between the treatments over the period of the study. There was a final increase of 0.36 min in the placebo group, 1.4 min in the treated group and a minor production of lactate during exercise in the treated group. Left ventricular shortening fraction and left ventricular ejection fraction showed a significant increase in the L-propionylcarnitine group (respectively P < 0.01 and P < 0.0001) whereas no difference was apparent in the placebo group. Stroke volume index and cardiac index showed significant increments in the treated group (P < 0.05) and systemic vascular resistance was lowered (P < 0.05). No haemodynamic variations were observed in the placebo group, and the clinical score showed a significant improvement in the L-propionylcarnitine treated group. In conclusion, L-propionylcarnitine treatment was shown to improve patient symptomatology and effort tolerance.

Adult↗
PubMed1994

[Hyperinsulinemia and cardiovascular risk].

A large body of evidence has been accumulating that insulin plays a role in coronary heart disease (CHD). Hyperinsulinemia has been considered a risk factor for CHD according to prospective studies. Cross-sectional studies found an association between hyperinsulinemia and prevalence of CHD, while population studies have shown that populations at increased risk for CHD are hyperinsulinemic. Strong relations between hyperinsulinemia and atherosclerotic coronary lesions have been demonstrated by angiographic studies. It has recently been observed that also patients with microvascular angina are hyperinsulinemic. Several mechanisms have been proposed to explain the role of hyperinsulinemia in the development of atherothrombosis. Hyperinsulinemia is the consequence of insulin resistance, a defect in insulin-mediated glucose uptake. Experimental evidence suggests that insulin has actions that may promote atherosclerosis, which clinical studies suggest the existence of a metabolic syndrome characterized by the presence of major coronary risk factors in which insulin resistance is the common link.

Animals↗
PubMed1993

[Heart involvement in thymic neoformations: the role of magnetic resonance tomography. Experience in 3 cases].

Three paracardiac masses (1 thymic cyst, 2 thymomas) were studied by magnetic resonance imaging (MRI) using spin-echo, multi-echo, and gradient-echo sequences (cine-MR). MRI showed: a pedunculate cystic lesion, typical for thymic origin, in Case 1; cardiac and pulmonary infiltration, and 3 intracardiac metastases, in Case 2; cardiovascular compression but not infiltration, in Case 3. In 3/3 cases MRI was superior to transthoracic echocardiography (TTE), and in 2/2 MRI was superior to computed tomography (CT), not performed in Case 2 (allergy to contrast agents). MRI may be considered the most important technique to evaluate cardiovascular involvement by thymic neoplasms. MRI should be performed after TTE and makes CT unnecessary.

Adult↗
PubMed1992

Effectiveness and safety of a single intravenous bolus injection of tissue-type plasminogen activator in acute myocardial infarction. Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST) Investigators.

The efficacy of multiple intravenous bolus injections of tissue-type plasminogen activator (t-PA) in inducing rapid coronary recanalization in patients with acute myocardial infarction was previously demonstrated. In this Bolus Dose-Escalation Study of Tissue-Type Plasminogen Activator (BEST), the efficacy of 3 different doses of a single rapid intravenous bolus injection of t-PA (dute-plase, Wellcome Foundation, London) in inducing coronary patency (Thrombolysis In Myocardial Infarction perfusion grade 2 or 3) in 64 patients with acute myocardial infarction presenting less than 6 hours after onset of symptoms was investigated. At 60 minutes after administration of t-PA, the infarct-related coronary artery was patent in 9 of 17 patients (53%; 95% confidence interval [CI] 28 to 77%) after 0.3 MU/kg, in 14 of 23 (61%; 95% CI 39 to 80%) after 0.45 MU/kg and in 10 of 14 (71%; 95% CI 42 to 92%) after 0.6 MU/kg. At 90 minutes after t-PA, coronary patency was present in 9 of 17 cases (53%; 95% CI 28 to 77%) after 0.3 MU/kg, in 12 of 24 (50%; 95% CI 29 to 71%) after 0.45 MU/kg and in 10 of 13 (77%; 95% CI 46 to 95%) after 0.6 MU/kg. One patient in each dose group had a silent reoccluded infarct-related artery by 24 hours, and there were 2 clinical reinfarctions before discharge. No major bleeding events were observed. There were 5 hospital deaths, all unrelated to t-PA. A single intravenous bolus injection of 0.6 MU/kg of t-PA appears to be effective in inducing rapid coronary patency and to be safe in patients with acute myocardial infarction.

Adult↗
PubMed1992

Gallopamil and diltiazem: a double-blind, randomized, cross-over trial in effort ischaemia.

The aim of this study was to evaluate the efficacy and possibly the mechanism of action of gallopamil and diltiazem in a double-blind crossover trial in patients with effort ischaemia. Twenty male patients (mean age 57 +/- 6 years) with documented coronary atherosclerosis and exercise-induced ischaemia (ST depression greater than or equal to 0.15 mV) completed the study, which consisted of four 7 day periods. At the end of each period a multistage bicycle exercise stress test was performed under placebo (first and third periods) and randomly under gallopamil (50 mg t.i.d.) or diltiazem (90 mg t.i.d.) in the second and fourth periods. Both drugs significantly increased time to ischaemia (0.15 mV ST depression) as compared to placebo, from 7.9 +/- 1.7 min to 8.9 +/- 1.1 min (diltiazem) and 9.1 +/- 1.6 min (gallopamil) with no significant difference between the two drugs, and reduced the maximal extent of ST shift from 0.18 +/- 0.08 mV to 0.13 +/- 0.04 mV (diltiazem) and 0.12 +/- 0.05 mV (gallopamil). Analysis of the results from the whole population showed that the beneficial effect did not appear to be related to any specific parameter. Individual analysis showed that 13/20 patients under gallopamil and 13/20 under diltiazem increased time to ischaemia, while this was unchanged or reduced in the remainder. A positive correlation between changes in time to ischaemia and changes in rate x pressure product at ischaemia was found in both those administered gallopamil (R 0.80, P less than 0.01) and diltiazem (R 0.65, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗