Cardiologia (Rome, Italy)最新文献

Background: The aim of this study was to evaluate the pathophysiological role of fibrinogen in patients with chronic or acute ischemic coronary syndromes on the basis of epidemiological and clinical evidences showing the importance of fibrinogen as a risk factor for cardiovascular diseases and atherosclerosis progression.

Methods: We evaluated the behavior of plasma fibrinogen in 310 hospitalized patients with 1) acute myocardial infarction (n = 98); 2) unstable angina (n = 87); 3) chronic ischemic heart disease (n = 75); and 4) in controls without myocardial ischemia (n = 50). Fibrinogen was evaluated, by using the Clauss method, on day 1 and 5 during in hospital-stay and at 6-month follow-up in patients suffering from acute myocardial infarction.

Results: Plasma levels of fibrinogen were higher in patients with chronic ischemic heart disease (335.3 +/- 81.2 mg/dl, p < 0.001) and especially in patients with acute myocardial infarction (454.72 +/- 69.5 mg/dl, p < 0.00001) and unstable angina (382.6 +/- 101.3 mg/dl, p < 0.00025) in comparison with controls (271.28 +/- 62.4 mg/dl). Q wave myocardial infarction showed higher levels of fibrinogen than non-Q wave (461.3 +/- 95.8 vs 422.5 +/- 71.3 mg/dl, p < 0.02). Patients with acute myocardial infarction showed a further increase in fibrinogen on day 5 in comparison with entry levels (525.88 +/- 87.3 vs 454.7 +/- 69.5 mg/dl, p < 0.00001) regardless of the fibrinolytic treatment. Patients who died (n = 6) or had severe arrhythmias (n = 4) during in-hospital stay as well as those with post-infarction angina (n = 20) showed higher fibrinogen levels.

Conclusions: Our results confirm the role of fibrinogen as a risk factor for ischemic heart disease, especially in patients with unstable angina and acute myocardial infarction. In the latter, elevated fibrinogen values seem also to be associated with a worsen prognosis during hospitalization.

Background: The aim of this study was to evaluate, in patients with chronic renal failure in hemodialysis and arterial hypertension, the effectiveness of a new angiotensin II receptor antagonist, the candesartan cilexitil, comparing it with losartan, the first of this new class of drugs.

Methods: We have selected 128 patients with chronic renal failure (92 males and 36 females, mean age 56 +/- 6 years) and arterial hypertension, subjected to hemodialysis 3 times a week, with hemodialytic seniority of 90 +/- 10 months. The inclusion criteria in the study were given from the presence, after 15 days of pharmacological wash-out, of values of diastolic blood pressure (DBP) > or = 95 mmHg and systolic blood pressure (SBP) > or = 150 mmHg, despite a hemodialysis correctly performed. Patients were divided into two groups whether they received single blind randomized candesartan cilexitil 16 mg or losartan 50 mg at hour 8.00 for a period of 8 weeks at the end of which, after a period of pharmacological wash-out of 15 days, the drugs were administered to inverted groups for other 8 weeks. After 4 and 8 weeks of treatment an evaluation of the anti-hypertensive effectiveness by means of medical complete visit and measurement of blood pressure were made. The statistical analysis was made by means of Student's t test for paired data.

Results: All the patients concluded the study. After 4 weeks of treatment SBP and DBP were reduced in the group with candesartan cilexitil with regard to baseline values (SBP 151.8 +/- 6.3 vs 159.8 +/- 5.1 mmHg, p < 0.05; DBP 93.6 +/- 4.5 vs 98.1 +/- 3.7 mmHg, p < 0.05). In the losartan group (SBP 151.8 +/- 6.3 vs 158.7 +/- 5.5 mmHg, p < 0.05; DBP 93.6 +/- 4.5 vs 97.5 +/- 3.8 mmHg, p < 0.05) no significant reduction in blood pressure values was observed compared with baseline values (SBP 158.7 +/- 5.5 vs 159.8 +/- 5.1 mmHg, NS; DBP 97.5 +/- 3.8 vs 98.1 +/- 3.7 mmHg, NS). After 8 weeks of treatment in the candesartan cilexitil group (SBP 128.3 +/- 5.9 vs 159.8 +/- 5.1 mmHg, p < 0.05; DBP 81.5 +/- 4.1 vs 98.1 +/- 3.7 mmHg, p < 0.05) and in the losartan group (SBP 151.7 +/- 5.1 vs 159.8 +/- 5.1 mmHg, p < 0.05; DBP 92.7 +/- 3.9 vs 98.1 +/- 3.7 mmHg, p < 0.05) blood pressure values were reduced in the same manner as at baseline. By comparing the two drugs, candesartan cilexitil proved to have a better antihypertensive effectiveness (SBP 128.3 +/- 5.9 vs 151.7 +/- 5.1 mmHg, p < 0.05; DBP 81.5 +/- 4.1 vs 92.7 +/- 3.9 mmHg, p < 0.05).

Conclusions: Our experience suggests that angiotensin II receptor antagonists may be a therapeutic remarkable option in patients with chronic renal failure in hemodialysis and arterial hypertension; the antihypertensive effect seems to be class-specific. Nevertheless, at least for our data, a better and more rapid antihypertensive results was obtained with candesartan cilexitil.

Background: Myocardial perfusion in the risk area during the acute phase of myocardial infarction has been extensively investigated over the last few years. The so-called "no-reflow" or "low-reflow phenomenon" (absence of myocardial perfusion despite patency of the infarct-related coronary artery) was shown to correlate with worse postinfarction remodeling, in particular when myocardial contrast echocardiography was used. The aim of this study was to determine, during routine coronary angiography performed before and after coronary angioplasty (PTCA) during the acute phase of myocardial infarction, the existence of the no-reflow phenomenon and its relation with ventricular remodeling, by evaluating the dye video density in the myocardial risk area. This confirmation by a different diagnostic technique may serve to highlight the role of myocardial perfusion as an index of prognosis in the clinical setting of acute myocardial infarction.

Methods: Twenty-six patients (23 males, 3 females, mean age 57 +/- 8.7 years) who underwent either rescue (n = 11, 42.3%) or primary PTCA, according to clinical indications, of the left anterior descending coronary artery during an acute anterior myocardial infarction and who did not have stenosis of the left circumflex or right coronary artery, were retrospectively selected from a 6 year intake. The extent of coronary stenosis was assessed using biplane quantitative coronary angiography, while end-diastolic and end-systolic volume indexes, together with regional wall motion, were computed from echocardiography performed in the first 24 hours and at 6 months. Patients were subdivided into two groups on the basis of dye video intensity in the risk area, as assessed from images obtained during left main coronary artery injections before and immediately after PTCA. It was used a subtraction technique (Group A: increased video intensity, n = 12; Group B: no change, n = 14), assuming that higher peak intensity reflects greater myocardial blood volume. Three patients in Group B with ineffective PTCA were excluded, so that the final number of considered patients was 11.

Results: The distribution of rescue PTCA was similar in the two groups (7 in Group A vs 3 in Group B, p = 0.13) as were clinical characteristics and therapeutic regimen. There was a significant time * group interaction for end-diastolic volumes (-4.6 +/- 23% in Group A vs +22 +/- 22% in Group B, p = 0.029), whereas end-systolic volumes showed a tendency to greater dilation in Group B (+19 +/- 28% vs +0.9 +/- 31% in Group A), although this difference was not significant (p = 0.27). No interaction was evident for increase in the vessel area (+46 +/- 12.5% in Group A vs +43.2 +/- 13.6% in Group B, p = 0.99), or for extent of regional dysfunction (+3.08 +/- 10.9 chords in Group A vs -2.5 +/- 9.5 chords in Group B, p = 0.50).

Conclusions: The detection of myocardial blood v