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Biomedical subjects

M C Herbst

Publications and source records attributed to M C Herbst.

At least 19 recordsLinked to original sources

Ventricular fibrillation induction using nonsynchronized low energy external shock during rapid ventricular pacing: method of induction when fibrillation mode of ICD fails.

Third-generation implantable cardioverter defibrillators (ICD) are frequently implanted with nonthoracotomy systems and provide noninvasive methods for electrical stimulation and ventricular fibrillation induction. These modalities facilitate postoperative testing of the ICD. Rapid right ventricular burst pacing via the defibrillator is commonly used for initiation of ventricular tachyarrhythmias. However, with the available third-generation devices, ventricular fibrillation (VF) induction may be impossible in up to 19% of the patients. In these cases, transvenous placement of a right ventricular catheter has been required to generate VF and appropriately evaluate the device. We report a new technique of noninvasive induction of VF using a low energy external nonsynchronized shock delivered during ICD fibrillation induction pacing. In three patients, after all efforts to induce VF by the Ventritex Cadence V-100 had failed, a 20 J nonsynchronized shock was delivered during rapid RV pacing. This resulted in VF on the first attempt in all patients. This noninvasive technique of VF initiation may provide a useful clinical approach to ICD testing that eliminates the costs and risks of an invasive procedure.

Adult↗

Registration as a pharmacist in South Africa.

This article discusses the professional pillar of pharmacy with particular reference to the powers and functions of the South African Pharmacy Council, the registration to practise and the cancellation of registration of pharmacists. It also deals with the registration of pharmacists of 'political returnees' in post-apartheid South Africa.

Black or African American↗

Beta-endorphin response to exercise and mental stress in patients with ischemic heart disease.

UNLABELLED: We compared symptomatic, hemodynamic and opioid responses of heart disease patients to exercise testing and a stressful public speaking task. Plasma beta-endorphins were measured at rest and immediately post stress. Nineteen of 50 patients had angina during exercise; 31 had asymptomatic ischemia. No patient had angina during the speech, but two had ECG changes and 39% had radionuclide changes indicating ischemia. Patients with asymptomatic ischemia on exercise had a significantly greater beta-endorphin response than those with angina. Public speaking elicited a significantly larger beta-endorphin increase relative to change in double product (an index of stress) than did exercise. CONCLUSIONS: (1) Patients with silent vs painful ischemia experience a greater beta-endorphin response to exercise. (2) beta-endorphin response to a speech stressor is greater than to exercise when controlled for an index of stress. (3) Increased beta-endorphin response to a speech stressor may partially explain the predominance of silent ischemia during psychological stress.

Aged↗

The relationship between plasma beta-endorphin, opioid receptor activity, and silent myocardial ischemia.

OBJECTIVE: To investigate the role of the opioid system in the pathophysiology of silent ischemia through opiate antagonism with naloxone, and to determine the reproducibility of resting and postexercise beta-endorphin levels in predominantly asymptomatic patients with coronary artery disease. DESIGN: Randomized, double-blind, placebo-controlled crossover trial. SETTING: A University hospital referral center. PATIENTS: Ten patients with prior evidence of silent exercise-induced ischemia were studied. INTERVENTION: An infusion of saline placebo or naloxone at two dose regimens of 0.015 mg/kg or 0.15 mg/kg before supine exercise testing during three separate occasions for each patient. OUTCOME MEASURES: Plasma beta-endorphin was measured at rest, immediately after exercise, and 5 min poststress. Timing and severity of angina and exercise hemodynamics were also determined. RESULTS: Seven of 10 patients reported no angina, whereas the other three experienced angina with placebo and after administration of naloxone at both doses. The severity and duration of angina was consistently noted to decrease in these patients after naloxone administration, especially after low-dose naloxone relative to placebo. There were no apparent correlations between beta-endorphin levels and the characteristics of angina in these three patients, nor between beta-endorphin and hemodynamic responses in all patients in the study. CONCLUSIONS: (a) naloxone failed to precipitate angina in this population of patients with silent ischemia; (b) naloxone appears to exert an analgesic effect at low doses; and (c) a variability of 5 pM at rest and 13 pM after exercise might be expected in predominantly asymptomatic patients due to random variation, which is comparable with results found in normal subjects.

Aged↗

Effects of 4 percent and 6 percent carboxyhemoglobin on arrhythmia production in patients with coronary artery disease.

In this study, we assessed the effects of exposure to 4 percent and 6 percent carboxyhemoglobin on ventricular arrhythmias in 41 subjects (nonsmokers) with documented coronary artery disease. We used a randomized, double-blind, crossover design. On day 1, a training session with no exposure, the baseline carboxyhemoglobin level was measured, and a supine bicycle exercise test was done. On days 2 through 4, subjects were exposed to room air, 100 parts per million (ppm)2 carbon monoxide (target, 4 percent blood carboxyhemoglobin), or 200 ppm carbon monoxide (target, 6 percent blood carboxyhemoglobin), and they then did a supine bicycle exercise test. Radionuclide ventriculography was performed at rest and during exercise. Ambulatory electrocardiogram recordings were made during the four consecutive days to determine the frequency of premature ventricular contractions at various intervals. The frequency of single premature ventricular contractions per hour during exercise was significantly greater on the 6 percent carboxyhemoglobin day than on the room air day (167.72 +/- 37.99 for 6 percent carboxyhemoglobin compared with 127.32 +/- 28.22 for room air, p = 0.03). The frequency of multiple premature ventricular contractions per hour was also significantly greater during exercise on the 6 percent carboxyhemoglobin day compared with the room air day (9.59 +/- 3.70 for the 6 percent carboxyhemoglobin day compared with 3.18 +/- 1.67 for the room air day, p = 0.02). Patients who developed increased arrhythmias during exercise on the 6 percent carboxyhemoglobin day were significantly older than those who had no increased arrhythmia, and, in addition, exercised longer and had a higher peak workload during exercise. No effect of carbon monoxide exposure was seen on the 4 percent carboxyhemoglobin day.

Aged↗

AIDS: a right to be informed.

Individuals have to assume some responsibility for their own health. Governments do, however, have a duty to ensure that their citizens are armed with the necessary information and education. At present there appears to be a serious degree of ignorance about sexually transmitted disease in general and AIDS in particular. The importance of disseminating information on this topic is discussed.

Acquired Immunodeficiency Syndrome↗

Production of arrhythmias by elevated carboxyhemoglobin in patients with coronary artery disease.

OBJECTIVE: To assess the effects of exposure to 4% and 6% carboxyhemoglobin on ventricular arrhythmias in patients with coronary artery disease. DESIGN: Randomized, double-blind, crossover design. SETTING: Exercise laboratory with an environmentally controlled exposure. PATIENTS: Forty-one nonsmokers with documented coronary artery disease. INTERVENTION: On day 1, a training session with no exposure, the baseline carboxyhemoglobin level was measured, and a supine bicycle exercise test was done. On days 2 to 4, patients were exposed to room air, 100 ppm carbon monoxide (target, 4% carboxyhemoglobin) or 200 ppm carbon monoxide (target, 6% carboxyhemoglobin), and they then did supine bicycle exercise with radionuclide ventriculography. Ambulatory electrocardiogram recordings were made during the 4 consecutive days to determine the frequency of ventricular premature depolarization (VPD) at various intervals. MEASUREMENTS AND MAIN RESULTS: The frequency of single VPD/h was significantly greater on the 6% carboxyhemoglobin day than on the room air day during the exercise period (167.72 +/- 37.99 for 6% carboxyhemoglobin compared with 127.32 +/- 28.22 for room air, P = 0.03). During exercise, the frequency of multiple VPD/h was greater on the 6% carboxyhemoglobin day compared with room air (9.59 +/- 3.70 on the 6% carboxyhemoglobin compared with 3.18 +/- 1.67 on room air, P = 0.02). Patients who developed increased single VPD during exercise on the 6% carboxyhemoglobin day were significantly older than those who had no increased arrhythmia, whereas patients who developed complex arrhythmias were also older and, in addition, exercised longer and had a higher peak workload during exercise. CONCLUSION: The number and complexity of ventricular arrhythmias increases significantly during exercise after carbon monoxide exposure producing 6% carboxyhemoglobin compared with room air but not after exposure producing 4% carboxyhemoglobin.

Age Factors↗

Aging and pain perception in ischemic heart disease.

Age is a recognized risk factor for coronary artery disease, but the relationship between age and silent ischemia is not well understood. We analyzed the data from 35 rest/stress radionuclide ventriculography examinations in patients with documented ischemic coronary artery disease who had experienced 1 mm ST segment depression accompanied by angina during exercise testing. An index of ischemic cardiac pain perception (PPI) was calculated by subtracting the time of onset of 1 mm ST segment depression from the time of onset of angina. The mean value of PPI was -97 +/- 311 seconds. PPI was significantly correlated with age (r = 0.37, p = 0.03). This suggests that as age increases, perception of pain during myocardial ischemic episodes becomes muted. This relationship remained significant when we controlled for the presence of medication and severity of disease (change in ejection fraction from rest to peak exercise). These findings suggest that age is an independent risk factor for a decreased perception of ischemic cardiac pain, and thus for silent myocardial ischemia.

Adult↗

Endorphins and pain perception in silent myocardial ischemia.

Evidence suggests that endogenous opioids, particularly the beta-endorphins and met-enkephalins, are closely involved in stress-induced analgesia and nociceptive pain control. Numerous investigations have been conducted to evaluate the role of opioids in silent vs symptomatic myocardial disease. There is good evidence to suggest that patients with asymptomatic ischemia have defective pain perception compared with those with angina; however, the precise role of the endorphin and enkephalin systems in this phenomenon remains to be elucidated. Possible sources for disparate study results include variation in patient populations, insensitive or improperly timed assay techniques, and differences in amount of ischemia.

Angina Pectoris↗

Effects of low-level carbon monoxide exposure on resting and exercise-induced ventricular arrhythmias in patients with coronary artery disease and no baseline ectopy.

The effects of acute elevation of carboxyhemoglobin (COHb) concentrations on resting and exercise-induced ventricular arrhythmias were evaluated in 10 patients who had ischemic heart disease and in whom no ectopy during baseline monitoring was noted. After an initial training session, patients were exposed to air, 100 ppm carbon monoxide (CO), or 200 ppm CO on successive days in a randomized, double-blind, cross-over fashion. After exposure to 100 and 200 ppm CO, venous COHb levels averaged 4% and 6%, respectively. Symptom-limited supine exercise was performed after exposure. Eight of the 10 patients had evidence of exercise-induced ischemia--either angina, 1.0 mm ST depression, or abnormal ejection fraction response--during 1 or more exposure days. Ambulatory electrocardiograms were obtained on each day and analyzed for arrhythmia frequency and severity. On air and CO exposure days, each patient had only 0-1 ventricular premature beat/h in the 2 h prior to exposure, during the exposure period, during the subsequent exercise test, and in the 5 h following exercise. In conclusion, low-level CO exposure is not arrhythmogenic in patients with coronary artery disease and no ventricular ectopy at baseline.

Aged↗

Depression and type A behavior pattern in patients with coronary artery disease: relationships to painful versus silent myocardial ischemia and beta-endorphin responses during exercise.

A sample of 45 patients with a history of coronary heart disease and documented myocardial ischemia during exercise testing were evaluated in an investigation of the possible relationships between psychological factors (depression and Type A behavior pattern), plasma beta-endorphin response and pain experience during maximal exercise-induced ischemia. Depression was assessed using the MMPI-D subscale, while Type A was evaluated using the Structured Interview. All patients developed ischemia during exercise as defined by ST-segment depression; however, only 18 patients reported anginal pain. Patients with high depression scores (MMPI-D greater than or equal to 70; n = 13) showed lesser increases in plasma beta-endorphin levels, tended more often to report anginal pain and rated pain as more severe during exercise than patients with low depression scores (MMPI-D less than 60; n = 18). Hemodynamic responses and severity of ischemia (assessed by ejection fraction changes and wall-motion abnormalities) did not differ between depression groups. Even after adjustment for group differences in exercise duration, depression was significantly associated with a lesser beta-endorphin response in the sample as a whole and, among patients reporting angina, with earlier pain onset and greater pain duration and severity. In contrast, when Type A versus B/X subgroups were compared, no differences in pain experience, beta-endorphin response or measures of ischemia were obtained. These findings suggest that in patients with ischemic heart disease, there may be a relationship between depression and anginal pain which may in part involve a blunted or absent beta-endorphin response.

Aged↗