Ventricular arrhythmias in ischemic heart disease

Article Abstract:

The leading cause of death in the United States is coronary artery disease. Most of these deaths occur at the time of a myocardial infarction, or heart attack, and arise from abnormal heart rhythms brought on by damaged heart tissue. Some of the cardiac deaths occur late after a heart attack, and most of these also arise from abnormal rhythms. The most common of these abnormal rhythms develop in the lower chambers of the heart, the ventricles, and the condition is known as ventricular arrhythmia. A summary of a conference held at UCLA to discuss various aspects of ventricular arrhythmias is presented. Ventricular arrhythmia in the immediate period of time surrounding a heart attack can be caused by a biochemical abnormality, such as abnormal levels in the heart muscle of potassium, calcium, or acid. Ventricular arrhythmia that occurs late after a heart attack, on the other hand, generally arises in the scar tissue left in the heart muscle, which disrupts the heart's normal electrical conduction. Among the strategies for treating ventricular arrhythmia tachycardia are drug therapy, surgery to remove the scarred portions of the heart muscle, and automated implantable defibrillators, and devices surgically implanted that deliver electrical shocks to the heart to terminate ventricular arrhythmia when it starts. None of these methods is perfect. For example, encainide and flecainide, two drugs thought to have great promise in eradicating myocardial infarction arrhythmias after a heart attack, were found to cause more than three and a half times as many deaths as not treating post-myocardial infarction patients at all. Much work has been done in understanding the mechanisms of ventricular arrhythmia tachycardia, but much remains to be done in determining the best means of treating it. (Consumer Summary produced by Reliance Medical Information, Inc.)

Care and treatment, Conferences, meetings and seminars, Complications and side effects, Heart attack, Ventricular fibrillation, Arrhythmia

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Myocardial ischemia during cocaine withdrawal

Article Abstract:

As the number of cocaine abusers increases, the number of cocaine-related cardiac events increases. Cocaine causes the heart rate and blood pressure to increase and blood vessels to constrict and spasm. These changes can lead to inadequate blood and oxygen supply to the heart muscle (myocardial ischemia), which can progress and cause destruction of heart muscle tissue (myocardial infarction, or heart attack). If the blood supply to the heart is already compromised by coronary artery disease, cocaine abusers are at a particularly high risk for myocardial infarction. Electrocardiography and treadmill exercise tests were performed on 21 male patients attending a cocaine abuse treatment program. Abnormal monitoring results indicative of silent myocardial ischemia occurred frequently in 8 of the 21 patients who were experiencing cocaine withdrawal. Most of these abnormal episodes occurred during the first two weeks of cocaine withdrawal. The electrocardiograph recordings from cocaine abusers were compared with those of normal patients and patients with stable and unstable angina (various patterns of chest pain associated with myocardial ischemia). Similar abnormal monitoring results were noted in only four percent of the patients with unstable angina and none of the patients with stable angina. On treadmill testing, one of 20 cocaine abusers had a positive test for myocardial ischemia. The results demonstrate that, particularly during the initial stages of cocaine withdrawal, cocaine abusers have an increased risk for silent myocardial ischemia. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Development and progression, Cocaine abuse, Cocaine, Drug withdrawal symptoms, Substance withdrawal syndrome

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Silent ischemia as a central problem: regional brain activation compared in silent and painful myocardial ischemia

Article Abstract:

The thalamus may play a role in intercepting pain stimulation from the heart to the central nervous system in patients who experience painless ischemia. Ischemia is a decrease in the blood supply to the heart muscle due to vessel blockage which frequently but not always produces chest pain called angina. Researchers compared brain scans of nine patients with a history of painful ischemia (group A) and nine patients with a history of painless ischemia (group B) before, during, and after drug-induced ischemia. There were increases in brain activity in both groups but in slightly different locations. Scans from group B patients showed greater increases in activity in the outer layers of the brain and in a section of the brain called the ventral cingulate than those of group A. Activity in the thalamus continued in both groups after the ischemia. Group A reported pain during the induced ischemia while group B did not.

Cerebral circulation, Measurement, Central nervous system

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