Isosorbide dinitrate inhibits platelet adhesion and aggregation in nonthrombolyzed patients with acute myocardial infarction.

BACKGROUND: Apart from their vasodilatatory properties, nitrates have been shown to inhibit platelet aggregation. The effects of nitrates on platelet adhesion have not been studied. Nonselected patients with acute myocardial infarction (AMI) have been suggested to gain no benefit from administration of nitrates. However, the importance of nitrates may be greater in a subgroup of nonthrombolyzed patients with AMI. HYPOTHESIS: Isosorbide dinitrate (ISDN) decreases platelet adhesion and aggregation in nonthrombolyzed patients with AMI. METHODS: Consecutive 48 men with AMI, not eligible for thrombolytic therapy because of late presentation (> 12 h), were prospectively randomized 2:1 to double-blind ISDN (mean dose 2.4 +/- 0.9 mg/h) (n = 33) or placebo (0.9% sodium chloride) (n = 15) infusion. All patients received aspirin. Blood samples were taken at baseline (no study medication) and 3 h into ISDN or placebo infusion. Platelet adhesion to collagen was measured in the ethylene diamine tetraacetic acid (EDTA)-platelet rich plasma by recording changes in light transmission with an optical aggregometer. Platelet aggregation was measured using the Born's method. RESULTS: Isosorbide dinitrate significantly decreased both platelet adhesion and aggregation. No effect was seen in the placebo group. CONCLUSIONS: In patients with AMI who do not receive thrombolytic therapy, ISDN effectively inhibits platelet adhesion and aggregation. These effects of nitrates may be of therapeutic and prognostic significance in this group of patients.

Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation.

OBJECTIVE: To assess the role of electrolyte imbalance in cardiac arrhythmias associated with congestive heart failure. DESIGN: Serum magnesium and potassium levels, urine magnesium excretion and the incidence of ventricular arrhythmias were assessed throughout the study. The patients who displayed complex arrhythmias after the first week of hospital medication were randomized 2:1 to double-blind magnesium supplementation or placebo. SETTING: The study was carried out in one municipal hospital, providing primary care. SUBJECTS: A total of 588 consecutive patients were screened for eligibility (clinical heart failure >/=6 months; NYHA class II-IV; left ventricular ejection fraction

Platelet adhesion is related to heart rhythm disturbances in the acute phase of myocardial infarction.

This study examines the relationship between platelet adhesion, aggregation and the occurrence of heart rhythm disturbances in 43 consecutive patients (mean age 58) admitted to a coronary care unit with acute myocardial infarction. Blood for platelet studies was taken prior to institution of any medication and heart rhythm was monitored (Holter) for 24 h after admission. The control group consisted of 22 healthy subjects (mean age 55 yr). Platelet adhesion to collagen was measured in EDTA-platelet rich plasma by recording the changes in light transmission in an optical aggregometer. Platelet aggregation was measured by the Born method. Platelet adhesion was increased in the group of patients with acute myocardial infarction as compared to controls and was significantly higher in the patients with complex ventricular arrhythmias (Lown 3-4b, n = 18) than in the patients with stable rhythm. Platelet aggregation in the patients with acute myocardial infarction did not differ significantly from the controls and was not related to heart rhythm disturbances. The causal relationship of increased platelet adhesiveness to collagen and heart rhythm disturbances in acute myocardial infarction remains to be established.

Platelet aggregation and arrhythmias after myocardial infarction.

We investigated the relationship between platelet aggregability and occurrence of complex arrhythmias in 72 males in the third or fourth week after the onset of myocardial infarction. The patients who displayed complex arrhythmias (n = 31), as opposed to those with stable rhythm (n = 41) showed higher platelet aggregability (48 +/- 27% vs 37 +/- 22%, mean +/- standard deviation, respectively, P less than 0.01). No differences were found with respect to plasma free fatty acids and excretion of catecholamines. It is suggested that, after myocardial infarction, increased platelet aggregability may contribute to the development of complex arrhythmias.

Echocardiographically detected left ventricular impairment after myocardial infarction is accompanied by latent complex arrhythmias.

The relationship between left ventricular (LV) wall motion disturbances (2D Echo) and latent complex ventricular arrhythmias (24-hr Holter ECG, Lown classification) in the late hospital phase of MI was investigated. A positive correlation was found between the extent of LV damage and the occurrence of complex arrhythmias expressed as the highest Lown class. Echocardiographic indices predictive of latent complex arrhythmias were derived. The most specific and predictive indices are: presence of dyskinesia, Heger index greater than 9, Heger index greater than 6 with LV enlargement, and number of hypo-, a- and dyskinetic LV segments greater than 4 with LV enlargement. Echocardiographic estimation of LV wall motion disturbances can be used as a method to identify patients threatened with major arrhythmias.