Usefulness of magnesium sulfate in stabilizing cardiac repolarization in heart failure secondary to ischemic cardiomyopathy.

Experimental heart failure is associated with cardiac magnesium loss, causing increased beat-to-beat variability in the action potential. Unstable repolarization contributes to sudden death, but no therapy has been shown to reduce repolarization variability safely. We sought to test whether a prolonged infusion of magnesium sulfate (MgSO(4); 40 mmol/24 hours) would normalize QT interval variability in patients with compensated heart failure. Fifteen patients (New York Heart Association class II to III; mean age 63 years) were enrolled in a placebo-controlled, double-blind study. Surface electrocardiograms were recorded and digitized at entry and at 48 and 168 hours (drug washout). Repolarization stability was assessed using an automated method measuring each QT interval in a 5-minute epoch. The QT variability index was derived as the ratio of normalized QT-to-normalized heart rate variability. Seven of 15 patients received MgSO(4). Mean heart rate and QT did not change in either group. The QT variability index was stable in the placebo group (-0.69 +/- 0.15 at entry, -0.71 +/- 0.22 at 48 hours, -0.70 +/- 0.18 at 168 hours), but decreased significantly in the treated group at 48 hours (-0.95 +/- 0.19 to -1.36 +/- 0.13, p <0.05 repeated-measures analysis of variance), returning to baseline at 168 hours (-0.84 +/- 0.18). Regression analyses showed that administration of MgSO(4) resulted in a stronger correlation between the QT and RR interval (p <0.01). Thus, MgSO(4) stabilizes cardiac repolarization in patients with compensated heart failure due to ischemic heart disease. Magnesium therapy may be useful in altering the proarrhythmic substrate in heart failure.

Effects of mental stress on coronary epicardial vasomotion and flow velocity in coronary artery disease: relationship with hemodynamic stress responses.

OBJECTIVES: This study examines the prevalence and hemodynamic determinants of mental stress-induced coronary vasoconstriction in patients undergoing diagnostic coronary angiography. BACKGROUND: Decreased myocardial supply is involved in myocardial ischemia triggered by mental stress, but the determinants of stress-induced coronary constriction and flow velocity responses are not well understood. METHODS: Coronary vasomotion was assessed in 76 patients (average age 59.9 +/- 10.4 years; eight women). Coronary flow velocity responses were assessed in 20 of the 76 patients using intracoronary Doppler flow. Repeated angiograms were obtained after a baseline control period, a 3-min mental arithmetic task and administration of 200 microg intracoronary nitroglycerin. Arterial blood pressure (BP) and heart rate assessments were made throughout the procedure. RESULTS: Mental stress resulted in significant BP and heart rate increases (p < 0.001). Coronary constriction (>0.15 mm) was observed in 11 of 59 patients with coronary artery disease (CAD) (18.6%). Higher mental stress pressor responses were associated with more constriction in diseased segments (rdeltaSBP = -0.26, rdeltaDBP = -0.30, rdeltaMAP = -0.29; p's < 0.05) but not with responses in nonstenotic segments. The overall constriction of diseased segments was not significant (p > 0.10), whereas a small but significant constriction occurred in nonstenotic segments (p = 0.04). Coronary flow velocity increased in patients without CAD (32.2%; p = 0.008), but not in patients with CAD (6.4%; p = ns). Cardiovascular risk factors were not predictive of stress-induced vasomotion in patients with CAD. CONCLUSIONS: Coronary vasoconstriction in angiographically diseased arteries varies with hemodynamic responses to mental arousal. Coronary flow responses are attenuated in CAD patients. Thus, combined increases in cardiac demand and concomitant reduced myocardial blood supply may contribute to myocardial ischemia with mental stress.

Mental stress as a trigger of acute cardiac events: the role of laboratory studies.

Mental stress has long been implicated as a potential trigger of myocardial infarction and sudden cardiac death. This article reviews research conducted in the past two decades utilizing laboratory studies to investigate behaviorally-induced pathophysiological effects (including increased cardiac demand, decreased myocardial supply, and impaired dilation of coronary resistance vessels), in patients with coronary artery disease. The clinical significance of mental stress-induced ischemia is supported by findings of a predictive relationship of mental stress-induced ischemia for ambulatory ischemia and subsequent cardiac events. Mental stress-induced ventricular fibrillation, ventricular tachycardia, and T-wave alternans are also being explored as possible markers of arrhythmic vulnerability in human and animal models. T-wave alternans comparable to exercise can be induced by an anger-like state in an animal model, and with mental stress in patients with implantable cardioverter-defibrillators. Future directions for research on mental stress and cardiac events are suggested, including further studies of mechanisms of mental stress-induced arrhythmia and ischemia, additional studies of the prognostic significance of stress-induced ischemia and T-wave alternans, and use of pharmacological and psychosocial treatments for preventing stress-induced cardiac events.

Predictors of psychosocial adjustment in patients with implantable cardioverter defibrillators.

Predictors of psychological distress/adjustment were examined in 25 patients following placement of ICDs. Patients completed a demographic questionnaire and a standardized questionnaire of psychological symptoms (i.e., Symptom Checklist-90 Revised; SCL-90-R). The number of discharges categorized by the patient as inappropriate and appropriate were also ascertained. The number of ICD discharges categorized as inappropriate and diminished levels of physical activity (r = 0.53 and 0.63, P < 0.01, respectively) did significantly relate to overall psychological distress. In addition, after controlling for age and prior psychiatric and physical health status through a stepwise multiple regression analysis, the occurrence of ICD discharges categorized as inappropriate and diminished physical activity continued to significantly predict overall psychological distress (R2 = 0.41, P < 0.01). However, the number of ICD discharges categorized as appropriate did not significantly predict overall psychological distress. The results of this investigation suggest that further refinement of the ICD could reduce the risk of exposure to potential psychological distress, and an analysis of prior and anticipated patient physical activity levels should be a factor when calibrating minimum ICD discharge threshold levels.

Adolescent personality disorder symptoms mediate the relationship between perceived parental behavior and Axis I symptomatology.

A study was conducted to investigate whether adolescent personality disorder symptoms mediate the relationship between perceived parental behavior and Axis I psychiatric symptomatology. The Parental Behavior Form, Personality Diagnostic Questionnaire-Revised, and Revised Hopkins Symptom Checklist (SCL-90-R) were administered to 187 first-year undergraduate students during their first week of college enrollment. One hundred fifty seven participants were readministered the SCL-90-R two months later. Results of correlational and hierarchical multiple regression analyses indicated that: (1) Adolescents' perceptions of parental acceptance/nurturance and harsh, controlling parental behavior were associated with baseline personality disorder symptom levels. (2) Perceived harsh parental control predicted both baseline and follow-up Axis I symptomatology. (3) In turn, baseline personality disorder symptoms were associated with Axis I symptom levels, both at baseline and at follow-up assessment after baseline Axis symptoms were accounted for. (4) Perceived parental behavior did not predict baseline or subsequent Axis I symptomatology after personality disorder symptom levels were accounted for. The present findings thus indicate that personality disorder symptoms completely mediated the relationship between adolescent perceptions of harsh, controlling parental behavior and Axis I psychiatric symptomatology.