SUMMARY Factors determining the symptoms of breathlessness and fatigue in patients with congestive heart failure were investigated by comparing the response to slow and fast exercise. Symptom limited oxygen consumption (maximal); minute ventilation, mean pulmonary capillary wedge pressure; and arterial blood gases, pH, and lactate concentrations were measured during treadmill exercise using a slow protocol in 25 men (age 34-67 years) with congestive heart failure (New York Heart Association class II-III). Ten of these patients were also exercised according to a rapid protocol. Exercise was terminated by fatigue in 23/25 patients after the slow test and by breathlessness in all patients after the rapid test. Exercise capacity (maximal oxygen consumption and exercise duration) was not related to resting or exercise pulmonary capillary wedge pressure or the change in pulmonary capillary wedge pressure during exercise, nor was there any difference in pulmonary capillary wedge pressure at the end of exercise within individuals between the fast and slow tests. Minute ventilation was greater (51 vs 43 1/min), peak exercise lactate concentration higher (3-7 vs 2-2 mmol/1), and the change in pH from the resting state was greater (0-06 vs 0 02) during the rapid test than during the slow test. The sensation of breathlessness in congestive heart failure is not simply related to raised pulmonary capillary wedge pressure, but may in part be due to stimulation of peripheral chemoreceptors in response to metabolic acidosis.The cause of exercise intolerance in congestive heart failure is poorly understood. Patients treated with diuretics are limited more by fatigue than by breathlessness. Several studies have suggested that fatigue is related to an inadequate oxygen supply to skeletal muscle,'-3 because during exercise patients with heart failure have a reduced cardiac output, an early increase in lactate concentration, and augmented limb oxygen extraction.3 Common experience suggests that untrained normal subjects performing rapid exercise (for example running) often stop because of breathlessness, whereas when they exercise slowly (for example walking) they stop because of fatigue. In this study we have investigated whether the response to exercise in patients with congestive heart failure is similar, and if so whether differences in the metabolic, haemodynamic, and ventilatory reRequests for reprints to Professor Philip A
Nineteen patients with chronic heart failure participated in a double blind crossover trial of captopril and prazosin -two drugs with differing neuroendocrine effects-to determine whether neuroendocrine changes could ex-
Aim-To determine whether measurement of serum troponin T concentration after first acute myocardial infarction can be used to identify patients with a left ventricular ejection fraction of < 40%, who have an adverse prognosis. Conclusion-Serum troponin T concentration measured 12-48 hours after admission for first myocardial infarction is a reliable, simple, quick, inexpensive, noninvasive method for identifying patients with a left ventricular ejection fraction of < 40% for whom there is a poor prognosis. (Heart 1998;80:223-225) Methods-Troponin
Aim-To determine whether elective direct current (dc) cardioversion of atrial fibrillation/flutter causes myocardial damage. Methods and results-Cardiac troponin T and creatine kinase were estimated 20-28 hours after dc cardioversion in 51 patients who received dc shocks for elective cardioversion of chronic atrial fibrillation/ flutter. Although creatine kinase was raised in 44 patients, cardiac troponin T was undetectable in all patients. Conclusion-Cardiac damage does not occur as a result of cardioversion. (Heart 1998;80:229-230) Keywords: cardioversion; troponin T; creatine kinase; atrial fibrillation Direct current (dc) cardioversion 1 revolutionised the management of cardiac arrhythmias. However, before the standardisation of outputs from external defibrillators there was controversy about the most appropriate strength of current to be used.2 Animal experiments have suggested that repeated high energy dc shocks result in myocardial damage.3 4 In humans, dc cardioversion causes a rise in the concentration of creatine kinase and its MB subfraction. [5][6][7] This observation, along with the electrocardiogram (ECG) changes (repolarisation abnormalities) sometimes seen after dc cardioversion, led to the suggestion that dc cardioversion causes myocardial damage. Most of the creatine kinase released after cardioversion comes from the chest wall skeletal muscles, 8 which also liberate the MB subfraction. Therefore, the extent that emergency dc cardioversion contributes to raised creatine kinase or its MB isoenzyme is unclear. The belief that myocardial damage might result from higher strengths of current may also have influenced recommendations about the choice of current strength. It remains uncertain whether dc cardioversion does actually cause myocardial damage.Cardiac troponin T is a cardiac specific protein component of the troponin/tropomyosin complex. 9 A rise in serum troponin T concentrations is specific for cardiac damage. It remains raised for up to 48 hours after myocardial injury, thus providing a wide time window. 9Currently available data suggest that the kinetics of cardiac troponin T release from acutely damaged myocardium are identical whatever the cause of damage. 10Our study was undertaken to determine whether there was any evidence of myocardial damage after elective dc cardioversion of atrial fibrillation/flutter by measuring concentrations of cardiac troponin T in patients undergoing dc cardioversion. MethodsFifty one consecutive patients undergoing elective dc cardioversion for atrial fibrillation/ flutter were entered into the study. None had chronic renal failure, acute myocardial infarction, or skeletal muscle disease. As described previously, 11 dc shocks were administered in increasing strengths of 100 J, 200 J, 300 J, and 360 J (only one shock of each strength), until either sinus rhythm was restored or 360 J was applied.A blood sample was taken 20-28 hours after dc cardioversion. Samples were centrifuged and analysed or frozen at −70°C until analysis (all analyses were p...
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