Biomedical subjects
Publications and source records attributed to J Porterfield.
We report the clinical, pathologic, and immunohistochemical features of a severe hypertensive patient with recurrent migraine-induced hypotension. The patient died of migraine-induced vasomotor paralysis despite prompt institutions of fluid and sympathomimetic and parasympatholytic agents. Postmortem study revealed autonomic ganglionitis and neuritis.
Hypertrophic cardiomyopathy is characterized by a nondilated, hypertrophied left ventricle in the absence of any overt cause. A possible role of adrenergic innervation or of cellular calcium regulation is suggested by the presence of hyperdynamic left ventricular function and by the clinical and symptomatic improvement seen in patients treated with beta-receptor antagonists or calcium antagonists. Therefore, we measured the density of calcium-antagonist receptors and beta-adrenoceptors in the atrial myocardium of 16 patients with hypertrophic cardiomyopathy and 19 patients with various other cardiac disorders. For comparison, we also measured the number of voltage-sensitive sodium channels. Calcium-antagonist binding sites, measured as the amount of dihydropyridine bound to atrial tissue, were increased by 33 percent in patients with hypertrophic cardiomyopathy (mean [+/- SD], 397 +/- 104 fmol per milligram of protein in patients with hypertrophic cardiomyopathy, as compared with 299 +/- 108 in patients with other cardiac disorders; P less than 0.01). The densities of saxitoxin-binding sites on voltage-sensitive sodium channels and beta-adrenoceptors were the same in the two groups, although the density of beta-adrenoceptors was higher in atrial samples from patients receiving beta-receptor antagonists (165 +/- 86 fmol per milligram of protein [patients receiving beta-blockers] vs. 85 +/- 60 [patients not receiving beta-blockers]; P less than 0.04). The increase in the number of calcium-antagonist receptors in hypertrophic cardiomyopathy suggests that abnormal calcium fluxes through voltage-sensitive calcium channels may play a pathophysiologic part in the disease.
Fungal mural endocarditis is a rare entity in which the antemortem diagnosis is seldom made. This case presentation describes a patient in whom the clinical diagnosis of Aspergillus mural endocarditis was made by echocardiography and by biopsy of a peripheral embolic lesion. This led to a combined medical and surgical approach to therapy.
From a population of 260 patients with malignant ventricular arrhythmia (ventricular fibrillation or ventricular tachycardia with syncope) we identified 52 (20%) who had infrequent ventricular premature beats during exercise testing and 48 hours of ambulatory monitoring. These patients underwent invasive electrophysiologic study utilizing programmed premature stimulation with up to three extrastimuli at currents of twice and three times middiastolic threshold. The end point for testing was nonsustained ventricular tachycardia (NSVT), defined as 3 to 20 propagated responses resulting from the last premature stimulus. A multiple response was obtained in 45 patients consisting of reproducible NSVT in 36 and sustained ventricular tachycardia in nine. The 36 patients with NSVT underwent 540 electrophysiologic tests with 18 antiarrhythmic agents. Suppression of the repetitive response was achieved in 31 of the 36 patients (86.1%). After an average follow-up of 21 months, one of 31 patients in whom the repetitive response had been abolished had recurrent arrhythmia. This contrasted with recurrence in two of the five patients in whom NSVT was still provoked. During the extensive testing, ventricular fibrillation was not induced. Sustained ventricular tachycardia occurred in 27 of the 540 tests (5.0%), but cardioversion was required in only 12 (2.2%). We conclude that NSVT constitutes a safe electrophysiologic end point for selecting an effective antiarrhythmic program in patients who have experienced malignant ventricular arrhythmia but in whom monitoring and exercise testing are inadequate to guide therapy.
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