Antianginal effect of conventional and controlled release diltiazem in stable angina pectoris.

Two preparations of diltiazem, controlled release (CR) given twice a day (b.i.d.) and plain given 4 times a day (q.i.d.), were compared in a multicentre, double-blind, crossover study in 41 patients with stable angina pectoris. Therapeutic efficacy was assessed with maximal exercise tests, patient recordings on nitroglycerine consumption and angina attacks. No significant differences between the CR and plain tablets were seen in any of the efficacy variables. Maximal workload significantly increased from 127 W on placebo to 146 W on CR tablets and to 147 W on plain tablets. Anginal attacks/week significantly decreased from 11.7 on placebo to 4.9 on CR tablets and to 5.0 on plain tablets. Consumption of nitroglycerine tablets/week significantly decreased from 6.3 on placebo to 2.6 and to 3.4 on CR and plain-tablets, respectively. The number or the seriousness of the adverse events did not differ between the groups. The results imply that diltiazem CR b.i.d. is equally potent and safe as conventional diltiazem q.i.d. in the control of stable angina pectoris.

Discriminant analysis of the standard 12-lead ECG for diagnosing non-Q wave myocardial infarction.

Discriminant analysis was performed on 12 standard lead data from 159 normal subjects (N) and 304 patients with first myocardial infarction (MI): the latter group consisted of 543 patients with acute non-Q wave MI (NQMI-group A), 68 patients with acute Q wave MI (QMI-group B) and 183 patients (group C) with recent (29) or old (154) QMI. A discriminant function was computed to separate optimally the larger group of QMI patients (group C) from N. A total of 7 features accounted for a specificity of 92% and a sensitivity of 89%. The classification model was then tested on patients with acute MI, regardless of the presence of Q waves (groups A and B); rates of correct classification were 72% for acute NQMI and 85% for acute QMI. The best measurements were voltages in the late portion of the T wave in aVR, V1 and V5, in early and late QRS in V2, at mid-QRS in lead II and in the second half of the P wave in V1. A weighted combination of these features with the coefficients of the discriminant function produced individual discriminant scores for each subject. Group-mean scores were 1.82 for N, -1.27 for acute QMI, -1.14 for old QMI and -.44 for acute NQMI, indicating that acute NQMI was "closer" to N than both acute and old QMI. QRS measurements from the 12-lead ECG were also used to derive the 45 criteria/33 point Selvester score in 53 patients with NQMI: 32% of NQMI were classified as MI with a score of 3 points or more (corresponding to a posterior probability greater than .50). These results were compared with those achieved by multivariate analysis using only QRS measurements: 56% of NQMI were classified as MI with a posterior probability threshold greater than .50. Associating a point score greater than or equal to 1 with criteria for ST-T abnormalities yielded a sensitivity of 72% at a specificity level of 95%. The results emphasize the presence of diagnostic information outside the initial part of QRS, the power of multivariate statistical procedures applied on continuous measurements and the potential benefit of discriminant scores for quantitative assessment of myocardial infarction.

16-lead ECG changes with coronary angioplasty. Location of ST-T changes with balloon occlusion of five arterial perfusion beds.

Percutaneous transluminal coronary angioplasty (PTCA) occlusion in five individual coronary artery distributions produced significant ST elevation ("current of injury") in 48/50 PTCAs in 46 patients. Four patients had PTCA of two separate coronary arteries. Two patients had no significant ischemic ST changes in the 16 simultaneous lead ECG and no chest pain with PTCA. The six limb leads were recorded from Mason-Likar locations modified by moving them centrally on the anterior torso; the V leads were recorded in standard locations, except V1 was moved to V3R. Four extra leads were placed as follows: (1) left axilla, (2) left subcostal margin, (3) V8, and (4) midback at the level of V4-V8. The left axillary and back leads discriminated diagonal and left circumflex (LCX) PTCAs from the others and from each other. V6 showed ST elevation in all LCX PTCAs and in only 10% of left anterior descending occlusions. V3R showed ST elevation in 82% of right coronary PTCAs. In 48/50 (96%) of PTCA occlusions the ST elevation was localized to the torso locations defined in Forward Model Simulations as specific for the arterial perfusion bed involved. These data strongly support the hypothesis that additional resolution and sensitivity to ischemic change is to be expected with a broader array of ECG leads.

Clinical efficacy of hydralazine in chronic heart failure: one-year double-blind placebo-controlled study.

In a placebo-controlled trial 62 patients with chronic congestive heart failure (CHF) (New York Heart Association class III) had hydralazine (149 +/- 11 mg daily) or placebo added to conventional therapy. During 12 months' follow-up 27 patients dropped out, 15 of 32 in the hydralazine group and 12 of 30 among the control subjects. The 1-year mortality rate was 28% in the hydralazine group compared to 27% in the control group. Symptomatic improvement was noted in both groups; however, it was gradually more pronounced in the actively treated group with a statistically significant difference between the two groups at month 12 (p less than 0.05). The hydralazine patients increased their exercise capacity 25%, from 53 +/- 3 watts at month 0 to 67 +/- 4 watts at month 12 (p less than 0.01). No improvement in exercise capacity took place in the placebo group. A significant improvement in chest x-ray examination was found with hydralazine (p less than 0.01) in contrast to a significant deterioration among the control subjects (p less than 0.05). Thus, we conclude that hydralazine used in chronic CHF has beneficial clinical effects during long-term treatment.

A controlled study of early discharge after uncomplicated myocardial infarction.

Out of 383 myocardial infarction (MI) patients aged below 70 years, 252 (66%) were judged after the third day in hospital to have had uncomplicated infarctions. These patients were allocated at random to two groups, one of which was given treatment for 8 days and the other for 15 days. No significant differences in mortality, morbidity or incapacity for work could be detected during the three-month period of follow-up. The findings thus support previous conclusions that early discharge from hospital after uncomplicated MI is not associated with greater risk for the patient than later discharge.

Long-term treatment with beta-blockers after myocardial infarction.

162 patients discharged from hospital after mycardial infarction were randomly allocated to two groups, one received alprenolol 400 mg daily and the other served as the control. The period of follow-up was two years and all other treatment given was standardized. The two groups did not differ with respect to risk factors for myocardial infarction, the course of the acute infarct or treatment during follow-up. After two years one patient in the group treated with alprenolol had died suddenly as compared to nine in the control group. During the same period four fresh infarcts had occurred in the alprenolol group compared to 15 in the control group. Both these differences were statistically significant. Only four patients were obliged to discontinue beta-blocker treatment because of suspected side-effects. Long-term post-infarction treatment with beta-blockers appears to be an effective form of secondary therapy without serious side-effects.