The delay between onset of symptoms and coronary care unit admission is decisive in the outcome of patients with acute myocardial infarction.To evaluate the influence of the factors that affect the delay in acute myocardial infarction treatment.Multicenter case-control study conducted by 118 coronary care units in Italy. The median and mean times in cases and controls were compared for decision time, home-to-hospital time, and in-hospital time, and the influence of several potential risk factors on the delay was evaluated by comparison of patients admitted more than 6 hours after onset with those admitted within 6 hours after onset.Among 5301 patients with acute myocardial infarction, 590 who came to a coronary care unit after 12 hours were considered cases. Controls included 600 patients treated within 2 hours, 603 between 2 and 6 hours, and 466 between 6 and 12 hours. The median decision time among cases was 50-fold higher than that of controls who presented within 2 hours. Home-to-hospital time and in-hospital time appeared to play a less important role. Among the patient-related variables, advanced age, living alone, low intensity of initial symptoms, history of diabetes, strong pain at onset of the infarction, occurrence of symptoms at night, and involvement of a general practitioner seemed to affect delay significantly.Interventions aimed at reducing the delay in acute myocardial infarction treatment should primarily focus on the help-seeking behavior of patients.

BACKGROUND:To investigate whether the abnormalities of coronary arterioles observed in association with hypertrophic cardiomyopathy represent a generalized phenomenon, both forearm and coronary vasodilator reserve were measured in 12 patients with hypertrophic cardiomyopathy. METHODS:Forearm vasodilator reserve was evaluated by measuring minimal forearm vascular resistance (Rmin, the ratio of mean intra-arterial pressure to peak forearm blood flow measured by venous plethysmography) under conditions of maximal postocclusive reactive hyperemia. RESULTS:In a subgroup (n = 5) of patients, the intra-arterial infusion of sodium nitroprusside combined with arterial occlusion did not produce additional vasodilation, indicating that the ischemic stimulus was indeed maximal. Coronary reserve was quantitated by measuring left ventricular blood flow (13N-ammonia and positron emission tomography) and coronary resistance at baseline and after intravenous dipyridamole (0.56 mg/kg). Rmin was significantly greater in patients than in a group of age- and sex-matched controls. The percentage change in coronary resistance after dipyridamole was significantly related to Rmin, whereas no correlation was found between change in coronary resistance and individual septal thickness values. CONCLUSIONS:Independent of cardiac hypertrophy, systemic and coronary arterioles of patients with hypertrophic cardiomyopathy are affected by an abnormality that may contribute to the clinical evolution of this syndrome.

Background: Exercise stress testing and dipyridamole infusion induce ischemic-like ST-segment depression in some of the patients with hypertrophic cardiomyopathy. The precise pathophysiologic meaning of these stress-induced ECG changes still appears elusive. The aim of this study was to assess the pathophysiologic meaning of these ECG changes.Methods: A high-dose dipyridamole test (two-dimensional echocardiographic and 12-lead ECG monitoring during dipyridamole infusion up to 0.84 mg/kg over 10 minutes) was performed in 22 patients with hypertrophic cardiomyopathy. In addition, regional myocardial blood flow was measured by means of N-13-ammonia and dynamic positron emission tomography in all patients at baseline and after intravenous dipyridamole (0.56 mg over 4 minutes).Results: After high-dose dipyridamole testing, seven of 22 patients (responders) had ST-segment depression over 0.2 mV from baseline while 15 of 22 (nonresponders) did not. However, echocardiographic monitoring during dipyridamole testing did not show regional or global dysfunction in any patient. Responders and nonresponders showed comparable values of septal thickness (19+/-1.6 vs 20+/-0.9 mm, P is not significant), posterior free wall thickness (10+/-0.6 vs 10+/-0.2 mm, P is not significant) and left ventricular end-diastolic diameter (45+/-2 vs 46+/-1.6 mm, P is not significant). Coronary vasodilator reserve (dipyridamole/baseline) was lower in responders than in nonresponders both in the septum (1.11+/-0.30 vs 1.72+/-0.53, P<0.01) and in the left ventricular free wall (1.36+/-0.39 vs 1.93+/-0.73, P=0.07). Coronary angiography performed in responders showed normal coronary arteries in all of them.Conclusions: The ST-segment depression elicited by dipyridamole in patients with hypertrophic cardiomyopathy is associated with a depressed coronary flow reserve even in the absence of angiographically detectable coronary artery disease. The flow reserve seems to be reduced also in nonhypertrophied myocardium, suggesting a primary vascular abnormality.

To assess regional coronary reserve in hypertrophic cardiomyopathy, regional myocardial blood flow was measured in 23 patients with hypertrophic cardiomyopathy and 12 control subjects by means of nitrogen-13 ammonia and dynamic positron emission tomography. In patients with hypertrophic cardiomyopathy at baseline study, regional myocardial blood flow was 1.14 +/- 0.43 ml/min per g in the hypertrophied (20 +/- 3 mm) interventricular septum and 0.90 +/- 0.35 ml/min per g (p < 0.05 versus septal flow) in the nonhypertrophied (10 +/- 2 mm) left ventricular free wall. These were not statistically different from the corresponding values in control subjects (1.04 +/- 0.25 and 0.91 +/- 0.21 ml/min per g, respectively, p = NS). After pharmacologically induced coronary vasodilation (dipyridamole, 0.56 mg/kg intravenously over 4 min), regional myocardial blood flow in patients with hypertrophic cardiomyopathy increased significantly less than in control subjects both in the septum (1.63 +/- 0.58 versus 2.99 +/- 1.06 ml/min per g, p < 0.001) and in the free wall (1.47 +/- 0.58 versus 2.44 +/- 0.82 ml/min per g, p < 0.001).In addition, patients with hypertrophic cardiomyopathy who had a history of chest pain had more pronounced impairment of coronary vasodilator reserve than did those without a history of chest pain. After dipyridamole, coronary resistance in the septum decreased by 38% in patients without a history of chest pain, but decreased by only 14% in those with such a history (p < 0.05). Coronary resistance in the free wall decreased by 45% in patients without and by 27% in those with a history of chest pain (p = 0.06).These results show that, in patients with hypertrophic cardiomyopathy, coronary vasodilator reserve is abnormal not only in the hypertrophied interventricular septum, but also in the nonhypertrophied free wall of the left ventricle. This finding suggests that the reduction in coronary reserve is not necessarily due to myocardial hypertrophy, but may be a primary defect.

It has been established that angiotensin II stimulation may limit the antihypertensive potential of diuretic therapy in some patients. It is less clear, however, whether renin-angiotensin II stimulation is the cause of the flat blood pressure dose-response relationship to diuretics. To investigate this, 75 out-patients with essential hypertension were treated with chlorthalidone 12.5, 25 or 50 mg o.d. for 3 weeks, in a double-blind, placebo controlled cross-over study.