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Biomedical subjects

R Hardoff

Publications and source records attributed to R Hardoff.

At least 73 records · Page 4Linked to original sources

Hyperbaric oxygenation for necrotizing (malignant) otitis externa.

Two patients with extensive necrotizing otitis externa have been treated by hyperbaric oxygenation. One patient had facial nerve palsy and the other suffered from skull base involvement. Due to severe side effects, the preferred combined intravenous antibiotic therapy was changed to monotherapy in one case and completely withdrawn in the second. This was done before the commencement of hyperbaric oxygenation, while the necrotizing infection was still active. Hyperbaric oxygenation therapy was followed by complete resolution of the necrotizing otitis externa, which did not recur. The pathogenesis of the disease and mechanisms by which hyperbaric oxygenation might be of benefit are described. We conclude that hyperbaric oxygenation should be considered as adjuvant therapy for necrotizing otitis externa whenever a therapeutic pressure chamber is available.

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Effect of isosorbide dinitrate on cardiac output in severe cardiac failure: relation to initial hemodynamics, ventricular volume, and the preload reserve mechanism.

Isosorbide dinitrate (ISDN) improves the clinical and hemodynamic state of patients with heart failure, but may cause dizziness and syncope. To characterize patients in whom cardiac output falls with high-dose nitrate therapy and to examine further the pathophysiology of the fall in cardiac output in these patients, we studies the effect of sublingual ISDN on forward cardiac output in 14 patients with severe cardiac failure (New York Heart Association grades 3-4). We examined systolic and diastolic left ventricular (LV) function from pressure and volume analyses of LV function. After administration of 15 mg ISDN, cardiac output was either unaltered or increased in 7 patients (Group 1) (11 +/- 12%, mean +/- SD), and decreased in 7 (Group 2) (-13 +/- 10%) (Group 1 vs. 2, p less than 0.002). Initial systemic arterial pressure, LV ejection fraction, wedge and LV transmural filling pressures were similar in both groups, but Group 2 patients had a lower systemic vascular resistance (p = 0.07) and tended to have a larger initial LV end-diastolic volume and increased end-diastolic compliance; following ISDN the decrease in LV filling pressure and end-diastolic volume was larger and the product of the changes greater (p less than 0.02). Thus ISDN decreases filling pressure and improves forward cardiac output in some patients with congestive heart failure, but large doses may decrease cardiac output in a subset of patients who have a lower systemic vascular resistance and a larger more compliant ventricle, maintaining forward blood flow predominantly by a preload reserve mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

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Early detection of infantile endocarditis by gallium--67 scintigraphy.

An infant with suspected soft tissue infection of the knee was studied by 67Ga-scintigraphy. In addition to knee and hip joint increased activity, heart uptake was also demonstrated prior to the development of clinical signs of endocarditis. The early detection and treatment resulted in satisfactory clinical resolution.

Endocarditis, Bacterial↗

Effect of the second-generation calcium channel blocking drug nisoldipine on diastolic left ventricular dysfunction in heart failure.

The effect of intravenous nisoldipine (0.12 microgram/kg/min) on diastolic left ventricular (LV) dysfunction was studied from simultaneous hemodynamic and radionuclide measurements in 12 patients with New York Heart Association class II to IV cardiac failure. The initial LV filling fraction was low, the peak LV filling rate normalized for end-diastolic volume was decreased, and the pulmonary capillary wedge pressure (PCWP) was high and associated with clinical shortness of breath. Nisoldipine produced an increase in LV filling fraction from 36 +/- 17% to 43 +/- 20% (p = 0.003). The increase in filling took place in both early and late diastole: peak early filling rate (PFR) increased in 11 of the 12 patients (p = 0.02) and late diastolic filling rate (atrial [A] wave in eight of them (NS). When the determinants of these changes, were examined further, it was found that in the control state PFR was inversely related to LV end-systolic volume (r = 0.77), whereas the A wave was related in exponential fashion to PCWP (preload) (r = 0.79). Nisoldipine did not change the slope of these relationships, and it did not alter the end-diastolic pressure-volume relationship, implying that inherent myocardial relaxation and distensibility were unaltered by the drug. In summary, nisoldipine improved measurements of diastolic LV dysfunction in patients with cardiac failure. This study illustrates the importance of considering ventricular loading conditions when analyzing and interpreting measurements of diastolic ventricular dysfunction. The measured changes in diastolic LV function during infusion of nisoldipine appear to be due to alterations in ventricular loading conditions rather than to a direct myocardial effect of the drug.

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Gallium 67 scintigraphy in the evaluation of Gardner's syndrome.

Seven patients with Gardner's syndrome--familial polyposis, desmoid tumors, and extracolonic manifestations--underwent gallium 67 (67Ga) scintigraphy. Gallium 67 was taken up by all desmoid tumors and skull osteomas. Three patients were considered clinically disease-free and scintigraphy was normal. Gallium 67 scintigraphy may be a useful adjunct in the evaluation of patients with Gardner's syndrome.

Adult↗

Solitary pericardial metastasis detected by 67Ga scintigraphy in a patient with fever of unknown origin.

67Ga scintigraphy was performed in a patient with fever of unknown origin. Left pneumonectomy had been performed two years previously for carcinoma of the lung. There were no cardiovascular or new pulmonary signs. Four weeks of in hospital investigation did not reveal the cause of the fever. 67Ga uptake was localized in the heart and subsequent autopsy demonstrated pericardial metastasis to be the cause of the prolonged fever. Fever of unknown origin is a rare presenting symptom of malignant pericardial involvement and 67Ga scintigraphy was crucial in its diagnosis.

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Effect of the second-generation calcium channel blocker nisoldipine on left ventricular contractility in cardiac failure.

We studied the acute effects of nisoldipine, a new second-generation calcium channel-blocking drug, on cardiac hemodynamics and left ventricular (LV) contractility in 10 patients with grade 2 to 4 cardiac failure. Pressures were measured from an arterial line and a flow-guided catheter in the pulmonary artery, cardiac output by thermodilution, and LV ejection fraction simultaneously by radionuclide ventriculography. Ventricular loading conditions were altered by sublingual nitroglycerin to facilitate construction of LV end-systolic pressure (radial stress)-volume and stress-shortening curves. Nisoldipine, given by continuous intravenous infusion (0.12 micrograms/kg/min), reduced mean arterial pressure (p = 0.001), systemic vascular resistance (p less than 0.05), and the double product, a measurement of myocardial oxygen demand (p less than 0.01). Cardiac index, stroke index, and LV ejection fraction increased in 8 of the 10 patients. LV contractility was initially greatly reduced and was unchanged or slightly decreased during the administration of nisoldipine. Emax, the slope of the end-systolic pressure-volume curve, was unaltered in half of the patients and decreased in the others (NS), whereas the end-systolic stress-shortening curve did not change. In summary, nisoldipine has a potentially useful acute hemodynamic profile in patients with cardiac failure; it increases forward blood flow in most patients, decreases the determinants of myocardial oxygen demand, and produces little measurable changes in the inotropic state of the left ventricle.

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Synergistic effect of captopril and dobutamine on left ventricular pressure-volume and pressure-shortening relations in severe cardiac failure.

The acute effects of captopril and dobutamine, alone and in combination, on left ventricular contractility were assessed from left ventricular end-systolic pressure-volume and pressure-shortening relations in 6 patients with severe end-stage cardiac failure. Dobutamine was given by constant intravenous infusion on two occasions 48 hours apart, on one of these occasions the patient also received oral captopril in a dose of 37 +/- 12 mg 6-hourly. Pressures and cardiac index were measured, and left ventricular volumes and ejection fraction computed from simultaneously recorded radionuclide ventriculography. Dobutamine alone did not cause a statistically significant increase in stroke index, stroke work index, cardiac index and ejection fraction, although pulmonary capillary wedge pressure and right atrial pressure fell (P less than 0.05). There was no change in systemic or pulmonary vascular resistance nor in arterial blood pressure. Following administration of captopril, diastolic arterial pressure decreased (P less than 0.05), and the dobutamine challenge produced a greater and significant rise in stroke and stroke work index (P less than 0.05) and cardiac index (P less than 0.01). The left ventricular contractile state was unaltered by captopril but appeared to increase with dobutamine and more so during combined therapy with captopril and dobutamine, indicating a synergistic effect of the two drugs when given in combination.

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Advantage of combined therapy with captopril and nitrates in severe congestive heart failure.

We compared the acute hemodynamic effects of captopril and nitrates in 11 patients with severe congestive heart failure and Grade IV cardiac disability. Pressures were measured using a Swan-Ganz catheter system; cardiac output and stroke index were measured by thermodilution, and left-ventricular (LV) volumes and ejection fraction were calculated simultaneously with the hemodynamic measurements from radionuclide ventriculography. Measurements were made in each of four treatment states: control, sublingual isosorbide dinitrate (ISDN) (5 and 15 mg), oral captopril (50 to 200 mg daily) and during combined therapy with captopril and ISDN. Captopril produced a fall in mean arterial pressure (P less than 0.01) from 81 +/- 14 to 72 +/- 13 mm Hg, and a rise in stroke index from 30 +/- 5 to 35 +/- 91/min per m2 (P less than 0.05), while LV ejection fraction increased from 18 +/- 5 to 21 +/- 7% (P less than 0.05). ISDN reduced mean arterial, pulmonary arterial, right-atrial and wedge pressure. The combination of captopril and ISDN produced a greater fall in mean arterial pressure, a further rise in ejection fraction to 22 +/- 8% (P less than 0.05), a fall in systemic (P less than 0.05) and pulmonary vascular resistance (P less than 0.01) and a rise in cardiac (P less than 0.01) and stroke work index (P less than 0.01), while the beneficial effects of ISDN on right-atrial, pulmonary arterial and wedge pressure were again achieved. LV contractility, assessed from end-systolic stress-shortening relations, was essentially unaltered or decreased very slightly. The study showed that combined therapy with captopril and nitrates produced acute hemodynamic benefits superior to those achieved by treatment with captopril or nitrates alone.

Blood Pressure↗

Effect of captopril on left ventricular end-systolic pressure-volume and stress-shortening relations in severe cardiac failure.

The effects of captopril on cardiovascular dynamics and left ventricular (LV) contractility were studied in 11 patients with severe congestive heart failure and very poor global LV function. Pressures were measured using a flow-guided catheter, cardiac output by thermodilution, and LV contraction and ejection fraction by simultaneous radionuclide angiography. Ventricular loading conditions were altered by sublingual isosorbide dinitrate to facilitate construction of LV pressure-volume and stress-shortening curves. Captopril decreased mean arterial pressure (p less than 0.02) and systemic vascular resistance, while stroke and cardiac index increased in most patients. Left ventricular ejection fraction increased from 18 +/- 5 to 22 +/- 7% (p less than 0.05), but contractility, assessed from end-systolic pressure-volume and end-systolic pressure-shortening relations, was unchanged or decreased slightly. Heart rate and double product also tended to decrease. In contrast, arteriovenous oxygen difference widened and calculated total oxygen consumption increased during captopril therapy (p less than 0.05). The study showed that captopril improved forward blood flow, total oxygen extraction, and LV ejection fraction following the decrease impedance to LV emptying but not at the expense of an increase in ventricular contractility. This makes captopril an attractive drug for patients with end-stage cardiac failure and a severely damaged myocardium.

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