Bradycardia due to anthracyclines.
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Biomedical subjects
Publications and source records attributed to M C Petch.
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Treatment with beta 1-selective antagonists causes selective sensitization of isolated strips of human atrial myocardium to the inotropic action of epinephrine and beta 2-agonists but not of norepinephrine. To determine whether beta 1-selective antagonist treatment alters the responsiveness of cardiac beta 2-adrenoreceptors in vivo, we measured the positive chronotropic responses to salbutamol injected into the right coronary artery. Ten patients treated with atenolol (50-100 mg daily) were compared with 10 patients not treated with beta-blockers. The mean dose required to cause an increase in heart rate of 30 beats/min was 2.29 micrograms (log dose 0.36 +/- 0.12 micrograms [mean +/- SEM]) in the atenolol-treated patients. In the non-beta-blocker-treated patients, the dose required to cause an increase in heart rate of 30 beats/min was significantly greater, 8.91 micrograms (log dose 0.95 +/- 0.11 micrograms) (p less than 0.005). We conclude that treatment with beta 1-selective beta-blockers leads to increased cardiac responsiveness to beta 2-adrenoreceptor stimulation. This may be the underlying mechanism of the beta-blocker withdrawal syndrome and may make the heart more susceptible to the adverse effects of epinephrine in situations of stress (e.g., myocardial infarction).
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To demonstrate the presence of functional cardiac beta 2-adrenoceptors in man, we studied the responses to intracoronary injections of salbutamol in three groups of six patients. We injected salbutamol, a selective beta 2-adrenoceptor agonist, into the right coronary artery to avoid peripheral vasodilator action and to stimulate the sinoatrial node directly. Salbutamol injections caused a sinus tachycardia. The same doses of salbutamol injected into the aortic root caused no change in heart rate, ruling out a systemic effect. The mean dose required to cause an increase in heart rate of 30 beats/min (IHR30) was 2.6 micrograms in the first group of six patients. In 12 other patients salbutamol was given after beta-blockade to confirm the beta 2-selectivity of the responses. Doses of practolol (beta 1-selective blockade) and of propranolol (beta 1- and beta 2-blockade) that had equal beta 1-blocking activity were used. In six patients who were given practolol, the mean IHR30 dose was 2.1 micrograms. In six patients who were given propranolol, the mean IHR30 dose was significantly greater at 64 micrograms (p less than 0.001, practolol vs. propranolol). This study demonstrates that direct cardiac beta 2-adrenoceptor stimulation in man has a positive chronotropic effect.
Intracardiac granulomas can cause complete heart block. A case of complete heart block is reported in a patient who had had paragonimiasis 30 years before and who had radiographic evidence of calcified granulomas in the heart and lungs.
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Forty patients with chronic isolated aortic regurgitation were studied by phase analysis of equilibrium radionuclide ventriculography to see whether this technique could detect changes in left ventricular (LV) function before the onset of symptoms. This technique was compared to the radionuclide ejection fraction and echocardiography. The severity of LV volume overload was assessed using the radionuclide regurgitant index. Patients with clinically severe aortic regurgitation had severe volume overload (high regurgitation index), increased echocardiographic left ventricular dimensions and significantly increased phase spread (loss of synchrony of wall motion) compared to mild and moderate groups. All but one had well maintained global left ventricular function assessed by the ejection fraction. All seven patients with definite symptoms had a marked increase in phase spread and severe volume overload.
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The severity of aortic regurgitation, as assessed by the radionuclide regurgitant index and Fourier amplitude ratio, was compared in 29 patients. Both methods were highly reproducible and agreed in patients with mild-to-moderate regurgitation. The regurgitant index fell with exercise. This change showed a linear relationship with heart rate, allowing the regurgitant index to be corrected for heart rate. There was general agreement between the radionuclide method and echocardiography, but the regurgitant index was unable to select patients with symptoms. The regurgitant index provides an overall guide to the severity of aortic regurgitation, but may be unreliable in the presence of deteriorating ventricular function.
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