Be smart, don't kick the heart.

Blunt chest trauma is a rare cause of cardiac pathology. Nevertheless, a variety of life-threatening cardiac diseases can be caused by blunt chest traumas. In this case report we describe a myocardial infarction associated with kickboxing. We also review the literature describing myocardial infarction associated with blunt chest trauma.

Abortion of acute ST segment elevation myocardial infarction after reperfusion: incidence, patients' characteristics, and prognosis.

OBJECTIVES: To study the incidence and patient characteristics of aborted myocardial infarction in both prehospital and in-hospital thrombolysis. DESIGN: Retrospective, controlled, observational study. SETTING: Two cities in the Netherlands, one with prehospital thrombolysis, one with in-hospital treatment. PATIENTS: 475 patients with suspected acute ST elevation myocardial infarction treated before admission to hospital, 269 patients treated in hospital. MAIN OUTCOME MEASURES: Aborted myocardial infarction, defined as the combination of subsiding of cumulative ST segment elevation and depression to < 50% of the level at presentation, together with a rise of creatine kinase of less than twice the upper normal concentration. A stepwise regression analysis was used to test independent predictors for aborted myocardial infarction. RESULTS: After correction for "unjustified" thrombolysis, 17.1% of the 468 prehospital treated patients and 4.5% of the 264 in-hospital treated patients fulfilled the criteria for aborted myocardial infarction. There was no difference in age, sex, risk factors, haemodynamic status, and infarct location of aborted myocardial infarction compared with established myocardial infarction. Time to treatment was shorter in the patients with aborted myocardial infarction (86 versus 123 minutes, p = 0.05). A shorter time to treatment, lower ST elevation at presentation, and higher incidence of preinfarction angina were independent predictors for aborted myocardial infarction. Aborted myocardial infarction had a 12 month mortality of 2.2%, significantly less than the 11.6% of established myocardial infarction. CONCLUSION: Prehospital thrombolysis is associated with a fourfold increase of aborted myocardial infarction compared with in-hospital treatment. A shorter time to treatment, a lower ST elevation, and a higher incidence of preinfarction angina were predictors of aborted myocardial infarction.

Recurrent pacemaker lead induced axillary subclavian vein thrombosis.

This report describes a patient with two recurrences of axillary subclavian vein thrombosis more than 1 year after implantation of a permanent transvenous pacemaker. Both recurrences were successfully treated with local thrombolysis.

Angiographic dose-finding study with r-hirudin (HBW 023) for the improvement of thrombolytic therapy with streptokinase (HIT-SK). Interim results.

To evaluate the efficacy and safety of hirudin, a direct thrombin inhibitor, in patients with acute myocardial infarction, a dose-finding, angiography study was carried out. After a pilot phase in 10 patients treated with a bolus of 0.1 mg.kg-1 and a continuous infusion of 0.06 mg.kg-1.h-1 (dose group I), two doses of hirudin, bolus 0.2 mg.kg-1.h-1 (DG II), and bolus 0.4 mg.kg-1 with 0.15 mg.kg-1.h-1 (DG III) were tested and compared with heparin as an adjunct to streptokinase and aspirin. This interim analysis was mandatory due to puncture-site related bleedings. Early and complete patency was achieved in 30% of 35 heparin patients, in 40% of 10 DG I, in 47% of 58 DG II and in 62% of 14 DG III patients. A dose-response relationship particularly between DG I and DG II, was also observed in the anti-thrombotic activity monitored by the aPTT. Apart from the catheter-related bleedings, there were low rates of serious adverse events.

How long should high-risk patients with acute anterior wall myocardial infarction be monitored?

In 143 patients with an acute anterior wall myocardial infarction, left ventricular ejection fraction was determined within 72 h of admission. Left ventricular ejection fraction was below 40% in 114 patients. In this group late ventricular tachycardia or ventricular fibrillation occurred in 30 patients (26%). A left ventricular ejection fraction below 40% identified all patients who developed any late ventricular tachycardia and a left ventricular ejection fraction below 30% identified all who developed late ventricular fibrillation. After discharge another 2 patients with late ventricular tachycardia were detected. Death between 48 h and 3 weeks only occurred in patients with a left ventricular ejection fraction below 30%. Thus in patients with an acute anterior wall myocardial infarction a left ventricular ejection fraction below 30% within the first 72 h after the acute event identifies a high risk for late ventricular tachycardia or ventricular fibrillation. The occurrence of late ventricular tachycardia showed a gradual increase during 3 weeks of monitoring and no cut-off point could be detected within this time-window.

Heart failure and hepatitis in a patient taking tocainide.

We report, for the first time to our knowledge, heart failure and liver abnormalities which developed after 2 months of treatment with tocainide.

Plasma levels of disopyramide after administration of conventional capsules and sustained-release tablets.

A study was carried out in 33 patients with myocardial infarction and complicating arrhythmias to compare plasma levels of disopyramide attained after administration of conventional capsules or sustained-release tablets. On Day 1, 29 patients started treatment wtih 600 mg disopyramide in 3 divided doses of conventional capsules. In 18, disopyramide plasma concentrations of 3 mg/l or more were achieved within 300 minutes after the first dose. On the second day, patients were allocated at random to receive treatment double-blind for 11 days with 500 mg disopyramide daily given either as conventional capsules (17 patients) or as sustained-release tablets (16 patients). Plasma concentrations were measured just before and 3 hours after the morning dose. Mean maximum and minimum concentrations in the conventional capsule group were 4.4 mg/l and 2.8 mg/l, respectively, compared to 4.3 mg/l and 3.0 mg/l, respectively, in the sustained-release tablet group. For the next 30 days all patients continued treatment with sustained-release tablets. Mean disopyramide plasma concentration measured 15 to 18 hours after the last dose was 2.8 mg/l. Myocardial function was estimated during and 1 week after discontinuing disopyramide treatment. The mean fractional fibre shortening (echocardiography) during treatment was 23% less than that 1 week after discontinuation. The mean PEP/LVET (systolic time interval recording) was 7% higher during treatment compared with 1 week after discontinuation. In 4 cases, mean ejection fraction, measured by scintigraphic methods, during treatment was 10% less than 1 week after discontinuation. Anti-arrhythmic effect was investigated by continuous monitoring in the first 12 days and by Holter monitoring during the 30-day ambulant period and 1 week after discontinuing disopyramide. A significant reappearance of warning arrhythmias could be detected after discontinuing disopyramide sustained-release tablets. No anti-arrhythmic effect was detected in 4 patients. Six patients had to be withdrawn because of side-effects. It is concluded that disopyramide sustained-release tablets 500 mg per day in 2 divided doses gives therapeutic plasma concentrations of 3 mg/l comparable with conventional capsules. A myocardial depressive effect is noted of about 10%.