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Biomedical subjects

C Brunelli

Publications and source records attributed to C Brunelli.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Hypercholesterolemia and coronary disease: intervention strategies].

The decision to treat hypercholesterolemia must take into account both the risk of death and myocardial infarction and the risk/benefit ratio of treatment. Nowadays there is convincing evidence that hypercholesterolemia in patients with previous myocardial infarction is an important prognostic factor: furthermore, the excess of risk due to cholesterol is consistently higher than that in the general population. Prospective studies demonstrated that cholesterol lowering treatment obtained either with diet or drugs can improve survival and quality of life in postinfarction patients. Experimental, clinical and angiographic studies suggested that cholesterol lowering therapy can produce both stabilization and regression of the atherosclerotic plaque. In view of this, the evaluation of cholesterol level must be part of the general work-up of patients with previous myocardial infarction. The satisfactory results obtained with diet suggest to try a dietary treatment in post-infarction patients with high cholesterol level before using drugs. Since there are no clear-cut upper values, the end point of treatment should be to lower cholesterol levels to the values recommended for the general population, although we believe that threshold values to be obtained in these subjects should be lower than those requested in primary prevention.

Anticholesteremic Agents↗
PubMed1991

[The effects of pharmacological treatment in asymptomatic left ventricular dysfunction].

It is clearly settled that the management of overt heart failure offers poor prognostic impact due to the advanced setting of the disease. Relief of symptoms, objective benefits, as testified by short-term hemodynamic improvements, are as a matter of fact not reliable prognostic markers. Myocardial dysfunction starts early in the natural history of many cardiac diseases, and runs through the steps of progressive wall remodeling, witnessed by quantitative and qualitative changes in cells, interstitium and connective tissue. Experimental studies offered keys to interventions modulated to oppose the pathophysiological changes present in early myocardial dysfunction. At present, medical therapy has made great strides in testing early myocardial dysfunction. Angiotensin-converting enzyme inhibitors, which retard ventricular dilatation and thus may lower myocardial oxygen consumption requirements seem to offer a unique prognostic profile. Preliminary pilot studies on them and some of many large-scale multicentre trials still in progress reached evidence that this class of drugs is by this time a cornerstone of medical therapy, useful to lower cardiac events-rate in patients with heart failure.

Adaptation, Physiological↗
PubMed1990

Ergonovine maleate test detects anginal patients with poorly reproducible exercise tests.

The aim of the study is to evaluate the reproducibility of exercise testing and to determine whether there is any correlation between the reproducibility of exercise test and response to the ergonovine maleate test. Thirty-eight patients with mixed angina and documented coronary artery disease underwent an ergonovine maleate test and four exercise tests on consecutive days in the same basal conditions. The ergonovine test was positive in 20 patients (Group I) and negative in 18 patients (Group II). There were no significant differences in the clinical and angiographic data of the two groups. All 152 exercise tests were positive. The variability of the response of the repeated tests was assessed by means of an analysis of the following parameters: heart rate, blood pressure, rate-pressure product, watts, and minutes were recorded at the onset of ischemia (ST decreases greater than or equal to 0.1 mV). Range (maximal-minimal obtained value), ratio between range and maximal obtained value, and coefficient of variation (standard deviation/mean of the four parameters) were calculated for each patient. The analysis of these values demonstrated that while the test was reproducible in some patients, a high individual variability was present in others. Moreover, the individual variability results were higher in Group I than in Group II, with a statistically significant difference for all considered parameters. In conclusion, it is possible to have a poorly reproducible exercise test in patients with mixed angina. The correlation between a positive ergonovine test and a poorly reproducible exercise test suggests that abnormal coronary vasomotion may sometimes be present during exercise and may affect the reproducibility of the test.

Adult↗
PubMed1990

Intravenous nifedipine prevents ergonovine-induced myocardial ischemia in patients with stable effort angina.

Twelve of 40 consecutive patients with effort angina, documented coronary artery disease, and a positive exercise stress test had a positive ergonovine test. ST-segment depression (0.1 mV) occurred in ten and ST elevation (0.1 mV) in two patients. During the ergonovine maleate test the rate-pressure product recorded at the onset of ischemia (ST greater than or equal to 0.1 mV) was significantly lower than that recorded during the exercise stress test. The reproducibility of the rate-pressure product at ischemia was displayed in every patient with a second test; then, a third test after intravenous nifedipine infusion (1 mg over 5 minutes + 1 mg over 55 minutes) was performed. Six patients had negative results; out of the remaining six, three exhibited a significant increase in the dosage required for provoking ischemia. Both systolic and diastolic blood pressure were reduced by nifedipine, while only a slight increase in heart rate occurred, so that the rate-pressure product at any ergonovine dosage was decreased by nifedipine. No differences in the ischemic threshold during exercise and during the ergonovine maleate tests (in washout and after nifedipine) were found in patients with a positive or negative response to nifedipine. The ergonovine test was positive in a sizable (30%) number of patients with stable effort angina. In these patients nifedipine was effective in preventing ergonovine-induced myocardial ischemia.

Angina Pectoris↗
PubMed1990

[Systemic fibrinolysis in patients with refractory unstable angina].

We tested the safety and the usefulness of intravenous fibrinolysis in 44 patients with refractory unstable angina, defined as persistence of ischemic episodes during 48-hour Holter monitoring (phase 1) despite maximal medical therapy. After fibrinolysis, recurrence of ischemia was recorded during 1 week of observation in CCU including 2 24-hour Holter monitoring at the beginning and at the end of this week (phase 2): 17 patients completed the observation period without either symptomatic or asymptomatic ischemic episodes (Group A); the remaining 27 patients continued to manifest ischemia (Group B). No bleeding complications occurred. Within a 6-month follow-up, 2 patients of Group A had recurrence of unstable angina while in Group B, 10 patients underwent CABG or PTCA for refractory angina, 6 other patients with refractory angina continued medical therapy, 1 patient had a myocardial infarction and 2 patients died (p less than 0.001). Phase 1: the duration of total ischemia (min/24 hours) was a relevant prognostic marker: higher duration correlated with adverse clinical outcome (p less than 0.01). Phase 2: in comparison with phase 1, duration of total ischemia was significantly reduced (p less than 0.001). A percent value expressing this variation was calculated for each patient: (min of ischemia in phase 2 - min of ischemia in phase 1/min of ischemia in phase 1). The variation thus obtained again gave information on the clinical outcome: the greater was the reduction, the lower was the risk of cardiac events (p less than 0.001). Our data suggest that: clinical stabilization may be obtained with the addition of fibrinolysis to conventional treatment; Holter monitoring bears prognostic information helpful in identifying patients who need further intervention.

Aged↗
PubMed1990

Hypertension as a risk factor for sudden cardiac death and nonfatal myocardial infarction. Working Group of CNR Study OD1.

To evaluate long-term prognosis during medical treatment of hypertension associated with angina pectoris, a total of 1083 patients with angiographically-documented coronary artery disease were followed for a mean of 66 months. At the end of the study, follow-up was complete in 98% of all patients. Of the 1083 patients, 132 (12%) had hypertension and 951 (88%) were not hypertensive. During the follow-up period, there was a total of 15 deaths (11.3%) among the hypertensive population (vs. 61 or 6.4% in the nonhypertensives) as well as a higher incidence of nonfatal myocardial infarction (9.0% in the hypertensives vs. 3.7% in the nonhypertensives) (Figure 2). Six-year cumulative survival was 84% in the hypertensive patients as compared to 92% in the nonhypertensives. Among risk factors, historical data, clinical and catheterization findings, the only noninvasively-obtainable independent predictor of prognosis using multivariate analysis was hypertension (Table 3).

Actuarial Analysis↗
PubMed1990

Comparison of low-dose aspirin and coronary vasodilators in acute unstable angina.

Episodic platelet activation has been shown to occur in unstable angina, and aspirin should have an important therapeutic role in the management of these patients. The response to aspirin alone or to aspirin in combination with vasodilators such as heparin and beta-blockers has been assessed in 41 patients with unstable angina. Therapy was added sequentially in the event of recurrence of transient myocardial ischemia. Patients were randomly assigned to two groups. Group 1 (21 patients) received an intravenous infusion of isosorbide dinitrate and oral diltiazem, and group 2 (20 patients) received intravenous aspirin (60 mg the first day and 20 mg on successive days). This dose of aspirin reduced serum thromboxane B2 from 160 +/- 88 ng/ml (mean +/- SD) to undetectable values (less than 6 ng/ml, p less than 0.01). If episodes of ischemic ST segment shift continued, the therapy of group 1 was added to that of group 2 or vice versa; if further ST segment changes were documented, intravenous heparin and oral beta-blockers were added; if episodes of myocardial ischemia persisted, urgent coronary arteriography and myocardial revascularization were performed. Nine patients in group 1 and six in group 2 (p = 0.8) had no further episodes of myocardial ischemia on their initial therapy; 12 additional patients had no further episodes when taking combined therapy of aspirin and vasodilators. Thus, the administration of aspirin alone was not superior to coronary dilators; 30% of all patients continued to have episodes of myocardial ischemia or had a myocardial infarction develop when heparin and beta-blockers were added. Myocardial infarction occurred in one patient on vasodilator therapy alone, in two on combined therapy, and in two on full therapy. These results suggest that in some patients, the stimulus to coronary thrombosis and vasoconstriction occasionally becomes so strong that it cannot be inhibited by certain antagonist drugs. The unstable tendency to continuation of ischemia or evolution to myocardial infarction is not related to the severity of the persisting stenosis. Those patients not promptly responding to combined therapy immediately from admission should have early coronary angiography and aggressive treatment.

Angina Pectoris↗
PubMed1989

Long-term survival in medically treated patients with ischaemic heart disease and prognostic importance of clinical and electrocardiographic data (the Italian CNR Multicentre Prospective Study OD1).

In order to study long-term survival in medically treated patients with ischaemic heart disease in our country and to evaluate the prognostic significance of clinical variables, 1083 patients less than 65 years old were followed up for a mean period of 66 months (min 36, max 93). All patients performed an exercise stress test and had coronary angiography. Vital status was known for 98.3% of the patients. The great majority were treated with calcium antagonists and nitrates. In the overall population, the annual cardiac mortality rate was 1.54%. On the basis of clinical variables, groups with a tenfold difference in mortality could be identified. The annual cardiac mortality was 0.29% in patients without myocardial infarction and effort ischaemia and reached 3.12% in those with extensive infarction and/or severe reduction of exercise tolerance. Among risk factors, only arterial hypertension was an independent predictor of mortality. According to angiographic variables, the highest mortality rate was 5.7% in patients with three-vessel disease and poor left ventricular function. When multivariate analysis was applied to clinically stratified subgroups, angiographic variables gave additional prognostic information on survival only in the subgroup with an intermediate prognosis. In conclusion (1) the annual cardiac mortality in our medically treated patients is low; (2) patients with very different prognoses may be identified on a clinical basis; (3) coronary angiography adds prognostic information only in moderately severe disease.

Adult↗
PubMed1986

Clinical application of monitoring techniques: hemodynamic monitoring.

In the diagnosis of myocardial ischemia continuous hemodynamic monitoring may contribute to detection of transient ischemia, to definition of location and to elimination of its pathogenesis, and to characterization of hemodynamic response to ischemia. It can be helpful in investigating the significance of negligible, non specific and/or short-lasting electrocardiographic changes accompanying typical anginal symptoms. Simultaneous right ventricular and left ventricular pressure monitoring gives information regarding biventricular interaction during episodes of transient ischemia: an early left ventricular dysfunction, with or without a late right ventricular impairment, a selective right dysfunction, and a simultaneous left ventricular and right ventricular impairment all represent the hemodynamic patterns associated with left, right and biventricular ischemia respectively. Monitoring of hemodynamic parameters related to myocardial oxygen consumption and the study of their changes preceding the onset of ischemia during both spontaneous and provoked episodes of ischemia, may help in identifying whether functional or organic factors or both are involved in the pathogenesis of transient ischemia in individual patients. Two principal hemodynamic patterns appear to be associated with transient ischemia: a) left ventricular and/or right ventricular impairment, usually beginning shortly before the onset of electrocardiographic changes, followed by a rapid recovery and often an overshooting, b) a sudden and sustained increase in systolic pressure and heart rate, simultaneous with the onset of ST-T changes. In both cases, the 'excitatory' pattern appears to be unrelated to pain.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMed1983

Impairment of myocardial perfusion and function during painless myocardial ischemia.

Left ventricular (or pulmonary and systemic arterial) hemodynamics were measured for a mean of 13.6 hours during continuous electrocardiographic monitoring in 14 patients admitted to the coronary care unit because of angina at rest. Of 293 episodes of transient ST segment and T wave changes identified, 247 (84%) were completely asymptomatic. Sixty-three percent of asymptomatic episodes were associated with an elevation of the left ventricular end-diastolic or pulmonary artery diastolic pressure of 5 mm Hg or more; in 15% there were smaller elevations (2 to 4 mm Hg) and in 22% there were no changes or less than a 2 mm Hg elevation of pressure. The peak contraction and relaxation dP/dt (first derivative of left ventricular pressure) were reduced to 100 mm Hg/s or more in 84 and 81% of asymptomatic episodes, respectively. Great cardiac vein oxygen saturation measured in three patients showed an increased myocardial oxygen extraction similar to that seen in painful episodes, which preceded and accompanied asymptomatic electrocardiographic changes. These results indicate that asymptomatic electrocardiographic changes represent transient myocardial ischemia. Comparison of asymptomatic and symptomatic episodes revealed that asymptomatic episodes were generally shorter (253 +/- 159 versus 674 +/- 396 seconds, probability [p] less than 0.001) and produced less impairment of left ventricular function: there were smaller elevations of left ventricular end-diastolic or pulmonary artery diastolic pressure (5.9 +/- 5.0 versus 16.5 +/- 6.9 mm Hg, p less than 0.001), and smaller reductions of peak left ventricular contraction dP/dt (252 +/- 156 versus 395 +/- 199 mm Hg/s, p less than 0.001) and relaxation dP/dt (259 +/- 191 versus 413 +/- 209 mm Hg/s, p less than 0.001). In individual patients, however, asymptomatic and symptomatic episodes of similar duration and severity were observed. The duration and severity of ischemia appear important for the genesis of anginal pain, but additional factors must be involved.

Adult↗
PubMed1982

[The role of spasm in angina pectoris, myocardial infarction and sudden death. Indications for future research and treatment].

Recent concepts on the role of coronary artery spasm and other forms of vasoconstriction in coronary artery disease are studied with particular reference to episodes of transient ischemia and their therapeutic implications. The possible contribution of spasm and other obstructive mechanisms such as platelet agregation, to the different forms of angina, myocardial infarction and sudden death, is analysed in the light of clinical observations, some of which have not previously been reported. Based on these concepts and clinical considerations, new orientations for future research and treatment are suggested. In our series, long term treatment of coronary artery disease with the association of nitrate derivatives are suggested. In our series, long term treatment of coronary artery disease with the association of nitrate derivatives and calcium antagonists has led to a reduction in mortality and in the incidence of myocardial infarction over periods ranging from 2 to 4 years.

Angina Pectoris↗
PubMed1981

Increased fibrinopeptide A formation and thromboxane A2 production in patients with ischemic heart disease: relationships to coronary pathoanatomy, risk factors, and clinical manifestations.

In 98 patients with ischemic heart disease (IHD), independent of their clinical status (previous myocardial infarction, spontaneous angina or effort angina), a hypercoagulable state (indicated by significant elevation of fibrinopeptide A plasma level) and an increased platelet biologic activity were observed. Moreover, plasma fibrinopeptide A concentration and platelet aggregation were remarkably higher in patients with frequently occurring spontaneous clinical manifestations (active disease) than in IHD patients with relatively quiescent symptoms. Abnormalities of blood clotting and platelet changes were not significantly altered by the presence of severity of coronary angiographic fixed obstruction in IHD. Multiple regression analysis indicated that hypercoagulability and increased platelet biologic activity were not a consequence of differences in risk factor patterns in IHD patients compared to control subjects.

Blood Coagulation↗