During ventricular pacing, LV pump function is maintained best (i.e., at SR level) when pacing at the LV septum or LV apex, potentially because pacing from these sites creates a physiological propagation of electrical conduction.

Excessive tiredness is one of the most prevalent premonitory symptoms of myocardial infarction and sudden cardiac death. This state is labelled as vital exhaustion and consists of three components: fatigue, increased irritability, and demoralization. Vital exhaustion has been found to be an independent risk-indicator of myocardial infarction in one prospective study and several case-control studies. It is as yet unclear whether the association between vital exhaustion and future myocardial infarction can be explained by confounding of (subclinical) coronary artery disease. Therefore, the present study investigates the predictive value of vital exhaustion for the occurrence of new cardiac events after percutaneous transluminal coronary angioplasty (PTCA), while explicitly controlling for the severity of coronary artery disease. Patients with a successful PTCA were followed during 1.5 years. A new cardiac event was defined as present if one of the following end points occurred: cardiac death, myocardial infarction, coronary bypass surgery, repeat-PTCA, increase of coronary atherosclerosis, or new anginal complaints with documented ischemia. Vital exhaustion was assessed using the Maastricht Questionnaire two weeks after hospital discharge. Participants of the present study were 127 patients (mean age 55.6 +/- 9.1; 105 men, 22 women). Fifteen (35%) of the 43 exhausted patients experienced a new cardiac event, whereas 14 (17%) of the 84 not exhausted patients had a new cardiac event (OR = 2.7; CI = 1.1-6.3; p = .02). Multiple logistic regression analysis revealed that vital exhaustion continued to be of predictive value when other significant risk factors for new cardiac events were controlled for (i.e., severity of coronary artery disease and hypercholesterolemia).(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

After identification of the artery supplying blood to the arrhythmogenic area, transcoronary chemical ablation of ventricular tachycardia was undertaken in three patients with incessant tachycardia in whom the other therapeutic options had failed. Sterile ethanol (96%) was given at a dose of 1.5 ml in two patients and a total of 6 ml in the third. The arrhythmia was cured in two patients and suppressed during a 1-month period in the third until new collateral blood supply to the arrhythmogenic area developed and ventricular tachycardia recurred. The procedure was then repeated successfully. supply to preserve electrical activity of the myocardial cells involved in the mechanism of the arrhythmia. Evidence has been presented supporting reentry in surviving cells in the infarcted area as the mechanism of ventricular tachycardia after myocardial infarction.9"10 By using selective coronary angiography and cold isotonic saline, we have demonstrated that it is possible to localize the arterial blood supply to the site of origin of ventricular tachycardia after myocardial infarction."1 After identifying that artery, transcoronary chemical ablation of ventricular tachycardia was subsequently undertaken in three patients. Patients and MethodsThree patients with incessant ventricular tachycardia in the chronic phase after myocardial infarction were studied (