Hemodynamic effects of intravenous flecainide in acute noncomplicated myocardial infarction.

Hemodynamic and ECG effects of intravenous flecainide were assessed in 10 patients with acute myocardial infarction and no symptoms or signs of heart failure. The dose was 2 mg/kg injected over a 15-minute period. R-R interval did not change, but PR interval and QRS increased significantly, 28% (p less than 0.0005) and 20% (p less than 0.05), respectively. Duration of P wave also increased significantly, 15% (p less than 0.02). Pulmonary wedge pressure increased 29% (p less than 0.005) and cardiac index and left ventricular stroke work index decreased 9% (p less than 0.05) and 20% (p less than 0.05), respectively. No significant change in mean aortic pressure and systemic vascular resistance occurred. Thus, intravenous flecainide has a mild and transient negative inotropic effect in patients with noncomplicated acute myocardial infarction. It did not induce ventricular failure in this group of patients but should be administered cautiously to patients with overt heart failure or severe conduction defects.

Clinical spectrum of "unstable angina".

In order to determine the natural evolution of different clinical types of "unstable angina", 167 patients were included in a prospective study. After angiography, 11 (6.5%) were excluded because they had no significant coronary lesions. The remaining 156 were sorted into different groups according to their clinical characteristics and were followed up for a period of 24 months at least. After that follow-up period, mortality and incidence of acute myocardial infarction (AMI) were as follows: angina of recent onset (Class III--IV NYHA): 8.5% (3/35) and 34.2% (12/35). Progressive angina: 7.4% (2/27) and 7.4% (2/27). Intermediate syndrome: 41.6% (10/24) and 37.5% (9/24). Prinzmetal's angina: 10% (1/10) and 10% (1/10). Post acute myocardial infarction angina: 35% (7/20) and 10% (2/20). Acute persistent ischemia: 2.5% (1/40) and 20% (8/40). Comparison of these figures pointed out significant differences (p less than 0.001 for mortality and p less than 0.03 for AMI incidence respectively). We conclude that it is clinically possible to identify different groups within the so-called unstable angina. Such a division not only allows for the creation of more homogeneous groups, but it contributes to a more rational therapeutic approach and also permits identification of high risk prodromes of greater complications, such as myocardial infarction or sudden death.

Natural history of unstable angina with medical or surgical therapy.

In order to establish the natural evolution of unstable angina under medical treatment and to determine the possible benefits of revascularization surgery, 113 patients were studied; 51 received medical treatment (24 with intermediate syndrome and 27 with progressive angina), and 62 others received surgical treatment (28 with intermediate syndrome and 34 with progressive angina). After a mean follow-up of 32 months, the mortality in the medically treated groups was 46 percent (11/24) with intermediate syndrome and 7 percent (2/27) with progressive angina (P less than 0.005), and the incidence of myocardial infarction was 38 percent (9/24) and 7 percent (2/27), respectively (P less than 0.01). Moreover, in comparing cases treated medically or surgically, the mortality was as follows: intermediate syndrome treated medically, 46 percent (11/24) vs 11 percent (3/28) in those treated surgically (P less than 0.005); and progressive angina treated medically, 7 percent (2/27) vs 9 percent (3/34) in those treated surgically (P = 0.85). The incidence of myocardial infarction was as follows: intermediate syndrome treated medically, 38 percent (9/24) vs 14 percent (4/28) in those treated surgically (P less than or equal to 0.056); and progressive angina treated medically, 7 percent (2/27) vs 12 percent (4/34) in those treated surgically (P greater than 0.55).