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It has been observed that in patients with ST-elevation myocardial infarction (STEMI) the presence of ST-segment depression (ST) in heterozonal electrocardiographic leads (remote STI) worsens the patient's prognosis. The aim of this study was to observe in an unselected population with a first STEMI the incidence of remote STI and the risk factors related to this condition.We evaluated retrospectively 350 patients with a first STEMI; we excluded from our analysis 139 patients because no data about their coronary anatomy was available. ST-segment depression in the heterozonal myocardium was considered significant if0.1 mV at 60 ms from the J point, in at least two electrocardiographic leads.Patients were classified according to the presence (group 1, 117 patients) or absence (group II, 94 patients) of remote ST. The two groups did not differ for age, sex and coronary anatomy. In group I we found more heterozonal wall motion abnormalities than group II (32 vs. 18%, p = 0.018). In this group there was a higher incidence of smokers (56 vs. 33%, p = 0.025) and less patients were treated with statins when the STEMI occurred (6 vs. 14%, p = 0.047). Patients with remote ST had higher total cholesterol (214.6 +/- 48.9 vs. 192.3 +/- 29.8 mg/dl, p0.001) and low-density lipoprotein cholesterol (138.7 +/- 40.7 vs. 123.2 +/- 22.9 mg/dl, p0.0001) levels. Conclusions. In patients with STEMI the presence of remote ST is rather frequent, and seems to indicate a real heterozonal ischemia, independently of an epicardial coronary stenosis of the non-infarct-related artery. Remote ST. is associated with a higher incidence of risk factors related to microcirculatory dysfunction, such as cigarette smoking, a worse lipid profile and less protective factors, such as the use of statins prior to acute myocardial infarction.

After acute myocardial infarction, the presence of ischemic preconditioning as a result of preinfarction angina has a protective role, limiting necrosis extent and guaranteeing greater myocardial functional recovery. The relationship between preinfarction angina, microvascular reflow, and myocardial function is poorly known. We hypothesized that after acute myocardial infarction patients with preinfarction angina have both microvascular integrity and myocardial function preservation.In 51 patients with a first acute myocardial infarction, we noninvasively assessed microvascular perfusion and coronary flow reserve with intravenous myocardial contrast echocardiography and investigated myocardial contractile recovery with low-dose dobutamine and 90-day follow-up echocardiography. Typical angina was present in 25 patients and absent in 26 patients during the 7 days preceding the myocardial infarction. Compared with those patients without preinfarction angina, patients with preinfarction angina showed a greater microvascular reflow extent and coronary flow reserve (respectively, 25.2% +/- 22.8% vs 48.3% +/- 23.3%, P.05, and 3.44 +/- 0.75 vs 1.95 +/- 0.67, P.0001), a better regional myocardial function, as expressed with wall motion score index in the risk area at dobutamine (1.67 +/- 0.61 vs 2.10 +/- 0.43, P.005) and at follow-up (1.72 +/- 0.56 vs 2.22 +/- 0.40, P.0001) echocardiogram, despite being similar in the first echocardiogram (2.60 +/- 0.28 vs 2.63 +/- 0.28, P = not significant), and significantly less pronounced left ventricular dilation at follow-up.Presence of preinfarction angina, because of the preconditioning effect, reduces myocardial damage and favors myocardial viability, limiting left ventricular remodeling. This beneficial effect seems to be at least partly mediated by the more preserved microvascular integrity and functional vasodilation after acute myocardial infarction.

After acute myocardial infarction the preservation of the microvasculature is a pre-requisite for myocardial viability, limited ventricular remodeling and a better prognosis. Intracoronary myocardial contrast echocardiography after acute myocardial infarction can detect the extent of microvascular damage. We hypothesized that intravenous myocardial contrast echocardiography after acute myocardial infarction treated with primary coronary angioplasty can predict the contractile reserve at low-dose dobutamine echocardiography, myocardial functional recovery and left ventricular remodeling.We studied 37 patients with a first acute myocardial infarction and submitted to primary coronary angioplasty. All patients underwent echocardiography on the day they had the acute myocardial infarction, intravenous myocardial contrast echocardiography with power Doppler imaging 2.9 +/- 0.5 days later and dobutamine echocardiography 3.7 +/- 1.2 days after the acute myocardial infarction. In all cases, an echocardiography was performed at 3 months of follow-up.At intravenous myocardial contrast echocardiography, 25 patients showed contrast enhancement (reflow) and 12 a sizeable contrast defect (no-reflow). Reflow patients were found to have a regional wall motion score index similar to that of the no-reflow patients on the first day echocardiogram (2.6 +/- 0.4 vs 2.8 +/- 0.2, p = NS), but this parameter was smaller than that of the no-reflow patients at dobutamine echocardiography (1.5 +/- 0.4 vs 2.6 +/- 0.2, p0.0001) and at follow-up echocardiography (1.5 +/- 0.5 vs 2.6 +/- 0.2, p0.0001). The sensitivity and specificity of intravenous myocardial contrast echocardiography in identifying myocardial functional recovery at follow-up were 80 and 64%, while the sensitivity and specificity of dobutamine echocardiography were 85 and 76%. In no-reflow patients the left ventricular volumes increased from the acute to the chronic phase (end-diastolic volume from 71.9 +/- 14.1 to 100.9 +/- 40.6 ml/m2, p0.0001, +28%; end-systolic volume from 43.1 +/- 10.1 to 61.1 +/- 30.1 ml/m2, p0.0001, +29%), while they remained constant in reflow patients (end-diastolic volume from 71.8 +/- 20.1 to 71.1 +/- 15.4 ml/m2, p = NS, -1%; and end-systolic volume from 39.9 +/- 11.9 to 36.3 +/- 12.8 ml/m2, p = NS, -8%).Intravenous myocardial contrast echocardiography is capable of identifying patients with a post-infarction contractile reserve and myocardial functional recovery; it also allows the early identification of patients prone to late left ventricular dilation, thus permitting a more aggressive diagnostic and therapeutic strategy.

We describe the occurrence of an intraparenchymal (thalamic) haemorrliage during a stress test in a hypertensive 52-year-old man who had suffered from myocardial infarction 3 months earlier. Common causes of spontaneous haemorrhage, such as arteriovenous malformation, aneurysms, neoplasm, bleeding disorders or vasculitis were excluded. This single neurological complication was observed from among 8000 exercise tests performed in our Institute from 1987 to 1993.

The aim of this study was to investigate the anti-ischemic and antianginal activity and the duration of the new dihydropyridine calcium blocker nisoldipine (NIS) in patients with stable angina pectoris. The research was carried out on 16 patients, all male, 41-68 (mean of 58) years of age, with stable angina pectoris and fixed ischemic threshold (variations15%). After a 10-day washout period, patients were randomized to treatment with either 10 mg of nisoldipine or placebo (PL), twice daily for 21 days, according to a double-blind, crossover design. Patients underwent maximal symptom-limited exercise testing at 10 W/min on a bicycle ergometer, twice during the washout period, and once at the end of each treatment period, 3 and 12 h after oral administration of the drugs. In comparison with placebo, nisoldipine increased the ischemic threshold (N, 704 +/- 45 s; PL, 548 +/- 35 s; p0.01) and anginal threshold (N, 766 +/- 44 s; PL, 699 +/- 42 s; p0.01) for at least 12 h, and the ST-segment depression significantly decreased at maximal work (PL, 2.4 +/- 0.1 mm; N, 1.8 +/- 0.2 mm; p0.01) and at maximal common work (PL, 2.4 +/- 0.1 mm; N, 1.15 +/- 0.2 mm; p0.01). Similar to placebo the rate-pressure product was not significantly changed at higher submaximal effort after N, but it was significantly increased at the level of ischemic threshold, suggesting an increase in coronary blood flow to ischemic zones. Nisoldipine possesses anti-ischemic and antianginal activity lasting at least 12 h. This activity seems to be due to an increase in coronary blood flow to ischemic zones.

Gallopamil (GSR) is a new calcium-channel blocker. The anti-ischemic activity of GSR was investigated in 12 patients with stable angina of effort, with fixed ischemic threshold (variations < 15%). After a 7-day washout period, patients were randomized to receive treatment with either GSR 100 mg or placebo twice daily for 7 days. Patients underwent maximal symptom-limited exercise test, 10 W/min on a bicycle, during washout (twice) and after the end of each treatment period. Patients were studied by electrocardiogram and the cuff method for determining systolic blood pressure. After treatment with GSR, ischemic and anginal thresholds were increased for at least 12 h in comparison with placebo (ischemic threshold: GSR 663 +/- 37, placebo 571 +/- 36, p < 0.01; anginal threshold: GSR 708 +/- 32, placebo 646 +/- 38, p < 0.05). Rate-pressure product was not changed at the same levels of exercise, but it was significantly increased during exercise at ischemic threshold. In conclusion, GSR possesses an anti-ischemic and antianginal activity lasting at least 12 h. This activity seems due to an increase of coronary blood flow to ischemic areas.

The aim of this study was to investigate the anti-ischemic activity of propionyl carnitine (PC) in 18 informed, volunteer male patients, aged 37-70, suffering from a typical stable effort angina. The study design was randomized, balanced, crossover, and double blinded. The study lasted 75 days. In the first 15 days of washout the patients performed two maximal symptom-limited bicycle tests to verify the repeatability of the parameters examined. Then one group received PC for 30 days 500 mg three times a day, and the other group received placebo (PL) three times a day. At the end of 30 days the groups exchanged treatments. At the end of each period, 2 hours after the last oral administration, the patients performed a maximal symptom-limited bicycle exercise test with increased loads of 10 watts/min. No significant differences were observed between the two tests performed during the wash-out period, for a 1 mm ST-segment depression time, for the time to the end of exercise, and for the rate x pressure product at the same experimental time. The oral administration of PC in coronary patients increased both the 1 mm ST-segment depression time and the time to the end of exercise. Furthermore, the drug reduced the ischemic depression of ST at maximal common work and at maximal work. After PC, the rate x pressure product was not significantly different in relation to placebo at submaximal and maximal exercise. Thus PC seems to have an antiischemiclike effect, probably related to its metabolic activity.