The effect of verapamil on left ventricular remodelling and diastolic function after acute myocardial infarction (the Verapamil Infarction Study on Remodelling and Relaxation--VISOR).

The VISOR is a double blind, randomized, placebo-controlled study aimed to assess the effects of early and prolonged administration of verapamil on the left ventricular geometry and diastolic function in patients with anterior acute myocardial infarction treated with thrombolysis. Patients with heart failure or ejection fraction < 45% were excluded. Within 12 hours from starting thrombolysis, 70 patients were given verapamil (5 mg/hour intravenously for the first 24 hours, followed by 120 mg t.i.d. perorally for 6 months) or equivalent placebo. Echocardiograms were performed on admittance, before discharge, after 3 months and 6 months. The following parameters were calculated: left ventricular volumes, ejection fraction, sphericity index, early (E) and late (A) transmitral peak flow velocities and time-velocity integrals with their ratios, deceleration time and half-time of E, isovolumic relaxation time (IVRT), and non-invasive time constant of ventricular relaxation (tau). The basal and the last available parameters were considered for statistical analysis. The effects of the treatment on the left ventricular volumes, ejection fraction, and sphericity index were not statistically relevant. Conversely, a reduction of E/A ratio (P < .05) and increases of A integral (P < .01), deceleration time and half-time of E, IVRT and tau (P < .05) were found in the placebo group and not in the verapamil group. No significant changes in the blood pressure, heart rate, PQ interval, and biochemical parameters were observed in the two groups. In conclusion, in patients with a thrombolysed anterior acute myocardial infarction and preserved systolic function, verapamil can prevent alterations of the diastolic function in absence of effect on ventricular remodelling, and has a good safety profile.

Gallopamil activity on asynergic viable myocardium in acute myocardial infarction: insights on stunned and hibernating myocardium.

The influence of the calcium antagonist gallopamil on the contractility of asynergic viable myocardium after acute myocardial infarction treated with thrombolysis was investigated by two-dimensional echocardiography. Sixteen patients with > or = 1 viable segment(s), identified during the low-dose phase (up to 10 micrograms/kg/min) of a dobutamine echocardiographic test (up to 40 micrograms/kg/min) performed 4-5 days after a first acute myocardial infarction, were given a gallopamil intravenous bolus (50 micrograms/kg) 12-24 hours later. Two-dimensional echocardiography was done before and 15 minutes after the bolus. A score index of 1 (normokinesis) to 4 (dyskinesis) and a 16-segment model were used. A segment was considered viable when a resting asynergy (score > or = 2) improvement of > or = 1 grade was seen during low-dose dobutamine. Follow-up echocardiograms were done 3-5 months later. A total of 30 viable segments were found; of these, 10 showed sustained improvement in contractility (group A) during high-dose dobutamine, while 20 exhibited a biphasic response returning to their basal contractile state (group B). After the gallopamil bolus, 9 of 10 group A segments improved their contractility, in comparison with 0 of 20 group B segments (P < .001). Infarct-related vessel significant (> or = 75%) coronary stenosis was present in the tributary vessel of 0 of 10 group A and of 20 of 20 group B segments (P < .001). At follow-up, 9 of 10 group A segments showed a spontaneous contractile improvement; of the 20 group B segments, 8 of 10 that underwent revascularization (7 angioplasty, 3 bypass graft) showed contractile improvement, in comparison with 0 of 10 segments not revascularized (P = .001). We conclude that gallopamil may reverse the contractile dysfunction of postischemic stunned myocardium in patients with acute myocardial infarction, whereas no effects are apparent on ischemic/hibernating myocardium.

Identification of viable myocardium early after acute myocardial infarction under beta-blockade by enoximone echocardiography.

The influence of the beta-blocker metoprolol on the capacity either of low-dose dobutamine echocardiography or the recently introduced enoximone echocardiography to detect viable dysfunctioning myocardium after myocardial infarction was investigated. Initial clinical experience would suggest that the phosphodiesterase III inhibitor enoximona could be an alternative pharmacological stimulation, inducing an increase in contractility in the presence or absence of beta-receptor stimulation. Ten patients with a baseline low-dose dobutamine-echocardiographic test (up to 10 micrograms/kg/min) positive for myocardial viability in > or = 1 segment(s), performed 4-5 days after a first acute myocardial infarction treated with rtPA, were randomized after the administration of intravenous metoprolol (15 mg in three 5-mg boluses) either to dobutamine (up to 15 micrograms/kg/min) or to an enoximone intravenous bolus (1 mg/kg over 5 min) under echocardiographic monitoring, in a crossover sequence, with a 24-h interval. The infarct related artery was patent (TIMI grade 2 o 3) in all the patients. Follow-up echocardiograms were performed 5-7 weeks later. Resting asynergy was found in 40 segments; of these, 17 were viable. All the viable segments remained unresponsive during the post-metoprolol dobutamine infusion, while improved their contractility during enoximone echocardiography. Two patients suffering from early post-infarction angina underwent coronary angioplasty successfully. Eight out of ten patients (2 revascularized and 6 not) showed contractile recovery in a total of 14 segments at the follow-up echocardiogram. Sensitivity, specificity and overall accuracy in predicting reversible dysfunction after acute myocardial infarction for enoximone echocardiography were 93, 85, and 88%, respectively. Our results support the value of enoximone echocardiography in the identification of myocardial viability after myocardial infarction, in patients treated with beta-blockers, which interfere heavily with the results of dobutamine echocardiography.

[Early echocardiographic identification of viable myocardium after acute myocardial infarct using inotropic agents: comparison of dobutamine and enoximone]. / Ricerca ecocardiografica precoce del miocardio vitale dopo infarto miocardico acuto con agenti inotropi: confronto tra dobutamina ed enoximone.

BACKGROUND: The reversibility of regional dysfunction early after acute myocardial infarction may be obtained with inotropic adrenergic stimulation, in particular during low dose dobutamine infusion, suggesting the presence of viable myocardium. The aim of this study was to determine whether viable myocardium can be identified by two-dimensional echocardiography after an i.v. bolus of enoximone-positive inotropic non-adrenergic drug, phosphodiesterase III inhibitor as well as during dobutamine infusion, in patients with acute myocardial infarction. METHODS: Twelve male patients, aged 57 +/- 10 years and treated with rtPA (100 mg i.v. in 180 minutes) within the first 6 hours of a first anterior myocardial infarction were studied. All patients underwent a dobutamine infusion (5 and 10 mcg/kg/min, 5 minutes per dose) 4 +/- 1 days after entrance, followed by an enoximone bolus (1 mg/kg over 5 minutes) 1 hour later. Echocardiography was performed before dobutamine and enoximone, during dobutamine, 10 minutes after enoximone and at 6 +/- 2 months follow-up. A Wall Motion Score Index (WMSI) was calculated as recommended by the American Society of Echocardiography. All patients underwent coronarography on days 9-11 post-infarction. RESULTS: Improvement in regional function of basally asynergic segments occurred in 8 patients during dobutamine infusion, as well as after enoximone i.v. bolus, and in 1 patient only during dobutamine infusion. Both dobutamine and enoximone tests were found to be negative in the other 3 patients. A decrease of WMSI was observed with both dobutamine and enoximone tests (from 1.84 +/- 0.32 to 1.73 +/- 0.31; p = .002 with dobutamine; from 1.84 +/- 0.32 to 1.70 +/- 0.27; p = .0132 with enoximone) with concordant wall motion changes between two tests in 73/84 (87%; K = 0.61) basally asynergic segments. There were no complications occurred during the study. Of 8 patients with positive response for viable myocardium to both tests, 6 had a patent and 2 an occluded infarct-related artery. However, in the latter a collateral circulation toward necrotic area was present. At follow-up improvement in regional function of basally asynergic segments, with a decrease of WMSI (from 1.74 +/- 0.23 to 1.59 +/- 0.24; p < .05), was observed in 4 of 8 patients with viable myocardium detected by either dobutamine or enoximone. CONCLUSIONS: 1) Viable asynergic myocardium may be identified early after acute myocardial infarction by enoximone bolus, as carefully and safely as by dobutamine infusion; 2) transient recovery of post-ischemic myocardial dysfunction may be obtained independently of beta-receptor stimulation.

Lack of correlation between transient myocardial ischemia and late potentials on the signal-averaged electrocardiogram.

The relation between transient myocardial ischemia and late potentials was investigated in 100 patients with coronary artery disease who underwent serial recordings of the signal-averaged electrocardiogram before, during and after dipyridamole infusion. During this test, 47 patients (group 1) developed transient myocardial ischemia (with ST elevation in 14 cases and ST depression in 33), whereas 53 patients (group 2) did not. Baseline signal-averaged electrocardiogram was abnormal in 20 patients (20%): a QRS duration greater than 115 ms was seen in 6 patients, a late potential (root mean square voltage of last 40 ms of QRS [RMS40] less than 25 microV) in 9, both abnormalities in 5, with no significant differences between groups 1 and 2 (26 vs 15%, respectively). In both groups, comparison of recordings obtained before, during and after dipyridamole test revealed no significant changes in QRS duration and RMS40. Absence of significant differences was also observed when patients with transient ischemic ST elevation or ST depression were examined separately. During the test, 100% of abnormal basal recordings remained abnormal and 98% of normal recordings remained within normal limits. In only 2 patients (from group 1) RMS40, which showed borderline values at baseline, decreased to abnormal values during dipyridamole test. These data suggest that electrophysiologic abnormalities induced by transient myocardial ischemia may not bear any relation with the substrate for chronic reentrant ventricular tachyarrhythmias, as reflected by late potentials on the signal-averaged electrocardiogram.

[Pharmacological therapy and prevention of recurrent ventricular tachycardia]. / Terapia e prevenzione farmacologica delle tachicardie ventricolari ricorrenti.

Treatment of recurrent ventricular tachycardia (RVT) is still difficult, as far as choice of antiarrhythmic agents, dosage, associations and statement of their effectiveness are concerned; the Authors report their experience on twelve cases of RVT. The diagnosis of ventricular tachycardia was confirmed by esophageal electrograms in four cases and by intracardiac recordings in two cases. Patients were controlled by clinical observation, continuous electrocardiographic monitoring and several recordings. Ambulatory electrocardiographic monitoring was carried out in ten patients. Two patients left the hospital spontaneously; therapy was found to be effective in the remainder. Four patients were treated with quinidine plus betablockers, for cases with quinidine plus amiodarone. The results of long-term follow-up suggest that combined pharmacological therapy with drugs of different classes may be successful in preventing recurrences of ventricular tachycardia. The Authors think that careful choices of adequate therapeutic programs and rigid criteria for the evaluation of results should be planned in apparent refractory RVT, before referring to invasive procedures.

[Mortality and hospital complications of the myocardial infarction after dismissal from the coronary care unit (author's transl)]. / Mortalita' e complicazioni ospedaliere dell'infarto miocardico dopo la dimissione dall'Unita' Coronarica.

259 patients affected by myocardial infarction were followed after their dismissal from the Coronary Care Unit. Monitoring rate, reached 14,3% as well as serious complications which were distributed equally during this period. Death was caused by cardiac decompensation (48.6%), serious arrhythmia (16.3%), cardiac break down (13.5%), repeated infarction (10.8%), sudden death (10.8%). In all cases the autopsy revealed serious cardiac damage and widespread coronary alteration. According to statistics, death and the onset of complications appear according to age 55 years, Peel's index 12, anterior infarction, presence of complications in the C.C.U. Important among such complications are: symptoms and clinical signs of decompensation, serious ventricular arrhythmia, advanced BAV and interventricular block. The AA. reached the conclusion for the necessity of installing areas of subintensive care for the benefit of subjects who presented serious complications during their stay in the C.C.U. (about 40% of the cases). It is foreseeable that these units will have twice as many beds as the C.C.U.

[Epidemiological and clinical observations on 300 cases of primary myocardiopathy]. / Osservazioni epidemiologiche e cliniche su 300 casi di miocardiopatie primitive.

In the period from 1968 to 1977, in the Departments of Cardiology of the S. Camillo Hospital, a study has been made about 200 cases of Congestive Cardiomyopathy (MPC) and 100 about hypertrophic obstructive (MP0). Congestive cardiomyopathies constitute 1.5% of hospitalizations with a constant trend in the long run. In comparing these two forms, Authors have noticed some differences in the symptomatology of clinical and instrumental signs: 1) in case of MPO prevail angina, syncope, ejection systolic murmur, left ventricular overload in the ECG; 2) in case of MPC they find more frequently heart failure, embolism, diastolic gallop, cardiomegaly, A/V and intraventricular conduction disturbs. The AA. conclude, in accordance with Goodwin's classification, that there is not an uniformity of these two kinds of cardiomyopathies.