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Biomedical subjects

D T Mason

Publications and source records attributed to D T Mason.

At least 91 records · Page 5Linked to original sources
PubMed1983

The qualitative effects of laser irradiation on human arteriosclerotic disease.

To determine the effects of laser irradiation upon human coronary atherosclerotic disease, coronary plaques were extracted from fresh human cadaver hearts. Seventy-four diseased artery samples were sectioned either transversely or longitudinally and subjected to laser treatment from argon-ion and carbon dioxide sources. The laser beam affected vaporization and patency in fibrous, lipoid, and calcified plaques as observed histologically. Calcified blockage showed greater extent of charred remnants following controlled thermal injury than did fibrous or lipoid obstructions. The area and depth of penetration varied directly with intensity and duration of photoirradiation and inversely with the density of the atherosclerotic tissue. This study supports further research work on the use of lasers to effect relief of atherosclerotic obstructions.

Coronary Disease↗
PubMed1983

Effect of combined nitroglycerin and dobutamine infusion in left ventricular dysfunction.

The immediate therapy of severe left ventricular (LV) failure after acute myocardial infarction (AMI) frequently requires simultaneous preload reduction, pump output augmentation, and maintenance of systemic blood pressure. Therefore the effects of intravenous nitroglycerin (NG) and dobutamine (DB) were evaluated in 12 patients with severe LV failure following AMI. Nitroglycerin achieved salutary lowering of abnormally elevated LV filling pressure (23 to 14 mm Hg, p less than 0.001) while DB markedly augmented LV pump function (cardiac index rose from 1.7 to 2.5 L/min/m2, p less than 0.005). Notably, the combined infusion of NG + DB simultaneously decreased preload (LV filling pressure 23 to 14 mm Hg, p less than 0.001) and markedly enhanced LV pump performance (cardiac index increased from 1.7 to 2.4 L/min/m2, p less than 0.001). Minor decline in mean systemic blood pressure with NG (72 to 66 mm Hg, p less than 0.05) was rapidly reversed by DB addition (69 mm Hg, p greater than 0.05). Both agents were well tolerated without clinical or ECG evidence of myocardial ischemia or dysrhythmias. Thus the principally venodilator effects of NG minimize systemic hypotension while salutary augmentation of cardiac function in AMI with LV failure is achieved by NG + DB.

Catecholamines↗
PubMed1983

Ethmozine suppression of single and repetitive ventricular premature depolarizations during therapy: documentation of efficacy and long-term safety.

This study reports a total of 1677 patient days' experience with the use of Ethmozine to suppress ventricular premature depolarizations. A total of 39 patients were studied on three placebo-controlled protocols. Ethmozine, given at a mean total daily dose of 830 mg +/- 318 mg on a dosing schedule of every 8 hours, resulted in a mean plasma Ethmozine level of 0.42 micrograms/ml +/- 0.28 micrograms/ml. In addition to reducing ventricular premature depolarizations from 11,049/24 hr during placebo to 2231/24 hr during Ethmozine therapy (80% reduction), the drug also resulted in a 95% reduction in paired forms and a 99% reduction in total runs of ventricular tachycardia. Ethmozine is extraordinarily well tolerated with only mild side effects of dizziness, perioral tingling, and euphoria, with no serious toxicity requiring discontinuation of therapy. Ethmozine demonstrates great potential as an effective drug in suppressing ventricular premature depolarizations with minimal side effects or toxicity.

Adult↗
PubMed1983

Increased exercise tolerance after nitroglycerin oral spray: a new and effective therapeutic modality in angina pectoris.

The prophylactic antianginal efficacy of nitroglycerin (NTG) oral spray was assessed in 20 patients with angiographically documented coronary disease and stable angina pectoris. The evaluation was by a randomized crossover trial involving treadmill exercise testing. On study day 1, a control treadmill exercise test was performed, followed 30 minutes later by a second exercise test 2 minutes after administration of either placebo (group A, 10 patients) or NTG spray 0.8 mg (group B, 10 patients). One week later, on study day 2, the patients again underwent control treadmill exercise testing followed by a second exercise test after either NTG spray (group A) or placebo (group B). NTG spray delayed the onset of anginal pain during exercise by a mean of 100 +/- 64 seconds (p less than 0.001) in 13 patients and prevented pain entirely in seven. Placebo did not significantly delay the appearance of angina and prevented chest pain in only one patient. NTG spray increased treadmill exercise duration by 31% before the onset of angina (p less than 0.001); placebo did not significantly alter the duration of exercise. NTG spray abolished in six patients and delayed in 14 patients the onset of exercise-induced ST-segment depression of 1 mm (p less than 0.001). Patients achieved a higher heart rate at peak exercise with NTG spray, and yet the maximal exercise-induced ST-segment depression of 2.1 +/- 1.0 mm during the control study declined to 1.3 +/- 0.9 mm on NTG spray (p less than 0.001). Placebo had no effect on exercise ST-segment depression. These data indicate that the oral NTG spray is an effective prophylactic for exercise-induced angina.

Administration, Oral↗
PubMed1983

Circadian rhythm of hourly ventricular arrhythmia frequency in man.

Three twenty-four hour electrocardiographic recordings from 164 untreated patients were analyzed. A clear, statistically significant, diurnal pattern in hourly ventricular arrhythmia frequency was found. It was consistent across days and between seven diagnostic groups. A high frequency Noon to 4:00 PM peak contrasted with a low frequency 1:00 AM to 5:00 AM trough with zero hourly frequencies not uncommonly present. These findings appear applicable to large ambulatory populations and may well influence the design of future investigations of modalities which alter ventricular arrhythmia frequency.

Aged↗
PubMed1982

The effects of calcium channel blocking agents on cardiovascular function.

The hemodynamic effects of calcium blocking agents are a composite of the various direct and indirect cardiac and peripheral vascular actions of these drugs on the individual determinants of left ventricular pump function. Calcium antagonists have been shown to have a direct negative inotropic effect, a direct negative chronotropic effect and a direct effect to produce relaxation of vascular smooth muscle and vasodilation. These agents may also elicit important indirect effects by an anti-ischemic action referable to both coronary arterial dilation and reduction in myocardial oxygen demand, as well as a baroreceptor-mediated reflex increase in beta adrenergic tone in response to vasodilation. The net result of these direct and indirect actions on cardiocirculatory dynamics is also dependent upon the individual calcium blocking agent administered, the dose and route of administration, and the underlying status of left ventricular function. Available data do not lead to a clear definition of the hemodynamic effects referable to calcium blocking agents that may be produced by the interaction of all variable factors. At present, however, it would appear that the direct negative inotropic and chronotropic actions of the calcium antagonists are offset by the reflex increase in beta adrenergic tone, in combination with the reduction in afterload produced by the peripheral vascular effects of these agents. Preliminary data suggest that certain calcium inhibiting agents may be useful in the vasodilator therapy of congestive heart failure. Nevertheless, the direct negative inotropic effects of these agents have resulted in clinically evident decompensation in cardiac performance in patients with advanced left ventricular dysfunction, and caution is warranted in the application of calcium blocking agents in this setting.

Angina Pectoris↗
PubMed1982

Vasodilator therapy of severe congestive heart failure: the special importance of angiotensin-converting enzyme inhibition with captopril.

Successful ambulatory afterload reduction therapy of severe chronic congestive heart failure (CHF) required the extensive evaluation of hemodynamic effects of vasodilator agents, precise characterization of differential cardiocirculatory actions, and objective confirmation of extended salutary improvements of the heart failure state. This article describes results of a series of investigations with the angiotensin-converting enzyme (ACE) inhibitor captopril (CPT) in several patients with severe CHF. CPT causes predominant peripheral venodilation, resulting in marked decline in elevated left ventricular preload and modest augmentation of the depressed cardiac output. These hemodymanic effects of oral CPT are similar to the effects of nitroprusside and prazosin on increased ventricular preload, but the latter vasodilators cause greater rise in low cardiac pump output. Importantly, the beneficial cardiocirculatory action of oral CPT provided prolonged cardiac benefits with symptomatic improvements confirmed by objective enhancement in left ventricular function documented by cardiac catheterization, echocardiography, nuclear scintigraphy, and treadmill exercise. Thus, ACE inhibition with oral CPT successfully provides marked long-term augmentation of cardiac performance and clinical status in refractory CHF.

Adult↗
PubMed1982

Comparative analysis of the hemodynamic actions of captopril and sodium nitroprusside in severe chronic congestive heart failure.

The hemodynamic actions of the systemic vasodilators parenteral sodium nitroprusside (NP) and oral captopril (CPT) were compared in 11 patients with severe chronic congestive heart failure (CHF). While two agents produced similar reductions in mean blood pressure (NP, 90 to 70 mm Hg vs CPT, 88 to 74 mm Hg, p greater than 0.05) and left ventricular (LV) filling pressure (NP, 27 to 14 mm Hg vs CPT, 24 to 15 mm Hg, p greater than 0.05), they produce disparate effects on LV pump performance. NP raised cardiac index 35% (2.0 to 2.7 L/min/m2, p less than 0.005), whereas CPT increased this index 16% (1.9 to 2.2 L/min/m2, p less than 0.001). Concomitantly, the 31% elevation of stroke index produced by NP (26 to 34 ml/beat/m2, p less than 0.001) was greater (p less than 0.05) than the 15% rise produced by CPT (26 to 30 ml/beat/m2, p less than 0.001). Simultaneously, stroke work index showed similarly greater augmentation, and total systemic vascular resistance declined more with NP. These findings suggest that oral CPT is a predominant ventricular preload-lowering agent primarily likely to improve dyspnea related to severe pulmonary congestion in patients with advanced chronic CHF.

Captopril↗
PubMed1982

Complementary combined captopril and terbutaline therapy in severe chronic congestive heart failure.

The hemodynamic effects of captopril (CPT) alone and in combination with the beta-adrenergic receptor agonist terbutaline (TBT) were evaluated in 10 patients with severe chronic congestive heart failure (CHF). The heart rate remained unchanged, while CPT lowered mean systemic blood pressure from 86 to 64 mm Hg (p less than 0.001) and decreased left ventricular filling pressure markedly from 27 to 19 mm Hg (p less than 0.001). The addition of TBT produced no further change in these variables (p greater than 0.05). Simultaneously, CPT augmented cardiac index (CI) from 2.1 to 2.9 L/min/m2 (p less than 0.001) and stroke index (SI) from 27 to 37 ml/beat/m2 (p less than 0.001). Concomitant CPT-TBT further raised CI to 3.2 L/min/m2 and SI to 40 ml/beat/m2 (both less than 0.001). Further, the CPT-effected decline in total systemic vascular resistance from 1577 to 841 dynes . sec . cm-5 (p less than 0.001) was not reduced additionally by CPT-TBT combination (p greater than 0.05). These results indicate than both CPT and TBT markedly augment cardiac function in CHF. Moreover, the salutary effects of the systemic vasodilator appear additive to the beneficial actions of the beta-adrenergic receptor agonist, thereby providing substantial augmentation of the function of the failing heart.

Adult↗
PubMed1982

Importance of follow-up medical and surgical approaches to prevent reinfarction, reocclusion, and recurrent angina following intracoronary thrombolysis with streptokinase in acute myocardial infarction.

Thirty-four patients with acute myocardial infarction (mean age 55 years) who received intracoronary streptokinase for coronary thrombosis were followed for a mean of 9.4 months (longest 25 months) following the procedure of percutaneous transluminal coronary recanalization (PTCR). Twelve patients had undergone coronary artery bypass graft surgery (CABG), one had percutaneous transluminal coronary angioplasty (PTCA), and 21 received medical therapy. Among patients having CABG and PTCA, nearly 70% no longer had chest pain or reinfarction, and 62% were in New York functional class I status; there were no deaths, and there was only one reinfarction, in a patient who had graft closure. In contrast, 43% of medically treated patients had chest pain or reinfarction or had died on follow-up; only 32% of survivors were in class I functional status. Further, 71% of medically treated patients who were receiving warfarin had no chest pain and on reinfarction, whereas the majority (56%) of patients who did not receive either warfarin or antiplatelet agents either had chest pain or reinfarction or died. The importance of CABG/PTCA and anticoagulant therapy is stressed to prevent recurrent ischemia, reinfarction, and reocclusion following successful reperfusion by means of PTCR in acute myocardial infarction.

Angina Pectoris↗
PubMed1982

Reduction of submaximal exercise myocardial oxygen demand post-walk training program in coronary patients due to improved physical work efficiency.

To assess the effects of walk training on external work efficiency and the determinants of myocardial oxygen demand (MVO2), we measured total somatic oxygen consumption (VO2), heart rate (HR), and systolic blood pressure (SBP) in eight male coronary (CAD) patients during submaximal treadmill walking before and after at least 14 weeks of prescribed exercise. Each patient was tested before and after training at the individually determined horizontal treadmill speed that induced ischemic ST segment depression in the pretraining test. Although maximal oxygen uptake (VO2 max) did not increase significantly with training, submaximal exercise HR and the product of HR and SBP were significantly (p less than 0.05) reduced by 10% (120 leads to 108/min) and 16% (185 X 10(2) leads to 156 X 10(2)), respectively, and none of the patients had ischemic ECG changes after training. The reductions in the cardiac response to exercise were due primarily to a 10% decrease (18.9 leads to 17.1 ml/kg/min, p less than 0.05) in somatic oxygen requirements (VO2), indicating that the patients became more efficient walkers and reduced their MVO2 in proportion to the decreased total VO2. Thus, enhancement of external work efficiency, an extracardiac factor, can lessen myocardial energy costs (MVO2) and thereby raise the exercise threshold for cardiac ischemia in CAD patients even when aerobic capacity (VO2 max) is not increased.

Adult↗