We report here on a 73-year-old woman who ingested 3.6 g (40 mg x 90 tablets) of verapamil in a suicide attempt. On arrival, the patient was awake and well oriented. Two and a half hours after ingestion, she lost consciousness, as her heart rate and blood pressure began to decrease. Cardiac monitoring showed atrioventricular dissociation. Although she suffered from extreme hypotension, an echocardiogram revealed that the wall motion of the heart was almost normal, and cardiac output measured with a Swan-Ganz catheter was well preserved. The plasma verapamil concentration in this patient was 1499 ng/ml 4 h after ingestion. Hyperglycemia and hypokalemia, laboratory data revealed, continued for 18 h after admission. The patient was successfully resuscitated with intravenous saline, dopamine, and norepinephrine. Besides reporting on this case, we also report on a treatment for severe verapamil overdose.

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SUMMARY In order to investigate the relation between infarct size in acute myocardial infarction and left ventricular ejection fraction early after recovery, total creatine kinase released was calculated by the modified method of Sobel et al. (1972) from the serial determinations of serum CK activity; left ventriculography and selective coronary arteriography were performed at a mean of 2 months after the onset of infarction in 34 patients with acute myocardial infarction. Of 34 patients, 32 (94%) had left ventricular asynergy. In 21 patients with akinesis and/or dyskinesis, a significant correlation was found between the extent of thenon-contractingsegmentof theleft ventricle and left ventricular ejection fraction, indicating that the extent of the non-contracting segment contributes largely to reduction of ejection fraction in patients with myocardial infarction.A close inverse correlationwas also observed between theinfarct size and ejection fraction after anterior and after inferior infarction, though cardiac index was maintained over 2-0 1/min per m2 in all except 3 patients. The ejection fraction in patients with anterior myocardial infarction was lower than in those patients with inferior myocardial infarction with comparable values of total CK released. This was true even after exclusion of 6 patients with proximal right coronary artery lesions who might have had right ventricular necrosis as well as left, indicating that left ventricular function after infarction depends in part on the site of the infarct.Since Harrison (1965) In the present study, we attempted to estimate infarct size by calculating the total CK released from infarcted myocardium using the method of Sobel et al. (1972)

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The relation between the site and severity of coronary artery lesion and infarct size was investigated in 59 patients with acute myocardial infarction. All patients had no prior myocardial infarction and had at least one significant coronary narrowing (greater than or equal to 75%) in one of the major coronary arteries or in the first diagonal branch. Left ventriculography and selective coronary arteriography were performed on average 2.2 months after the onset of infarction to identify the site and severity of coronary narrowing and to assess the extent of the non-contracting segment (akinetic, dyskinetic, or aneurysmal). Thirty-four of 59 patients were studied enzymatically and total CK released was taken as an indication of infarct size. Non-contracting segment and total CK released in group L-I (narrowing proximal to the first diagonal branch) were significantly larger than those in group L-II (a coronary lesion distal to the branch). The data also indicate that the perfusion area of the first diagonal branch is as large as that of the left anterior descending artery below the first diagonal branch. In contrast to left anterior descending artery disease, the involvement of the right ventricular branch did not significantly influence the infarct size. However, infarct size was significantly larger in eight patients with the left ventricular branch of the right coronary artery supplying the predominantly large area of posterior wall of the left ventricle than in nine patients with small left ventricular branches. It was also shown that the severity of coronary narrowing does not correlate with the infarct size in either left anterior descending or right coronary artery disease.