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Biomedical subjects

D T Mason

Publications and source records attributed to D T Mason.

At least 127 records · Page 7Linked to original sources
PubMed1981

Evaluation of the effects of systemic nitroglycerin on perfusion of ischemic myocardium in coronary heart disease assessed intraoperatively by antegrade blood flow through intact saphenous vein bypass grafts.

To evaluate systemic nitroglycerin (NTG) effects on reduced perfusion of ischemic myocardium in coronary disease, intravenous NTG actions on coronary circulatory dynamics were directly assessed intraoperatively during aortocoronary bypass surgery in 24 patients. Thus metered antegrade blood flow was measured through 56 separate intack saphenous vein bypass grafts to analyze NTG perfusion response in the obstructed native coronary artery (CA). In 34 bypassed CA with proximal luminal diameter narrowing greater than 50% to 90%, NTG reduced (p less than 0.01) graft flow (GF) 82 to 63 cc/min, thereby indicating that NTG dilated proximal stenoses with resultant increased CA flow. In 11 bypassed CA obstructed greater than 90% to 100% with well developed collaterals distally, NTG decreased (p less than 0.05) GF 64 to 53 cc/min, thus indicating enhanced collateral flow. In contrast, in 11 bypassed CA obstructions greater than 90% to 100% without collaterals, that NTG increased (p less than 0.02) GF 91 to 100 cc/min indicated NTG nonresponsiveness of the severely diseased CA. Thus systemic NTG improves perfusion to ischemic myocardium subserved by diseased coronaries with less than 90% stenosis or by greater than 90% obstructed vessels with substantial collaterals distally.

Adult↗
PubMed1981

Ambulatory prazosin treatment of chronic congestive heart failure: development of late tolerance reversible by higher dosage and interrupted substitution therapy.

To evaluate whether long-term administration of the oral vasodilator, prazosin, in the ambulatory therapy of chronic refractory congestive heart failure (CHF) results in gradual attentuation of its marked salutary peripheral circulatory relaxing actions, 16 coronary heart failure patients receiving chronic prazosin, 16 mg daily, were assessed for the development of vasodilator tolerance for 12 months. In six of these patients such tolerance was documented after 7 months which was readily surmountable, thereby allowing continuation of effective chronic prazosin therapy. Each of the six tolerance patients underwent four forearm plethysmography studies: prior to chronic prazosin (study I; 4.0 mg study dose), after 7 months prazosin (study II; 4.0 mg), repeated following 1 additional week on higher effective prazosin dose of 32 mg daily (study III; 8.4 mg), and following 2 weeks of prazosin withdrawal (study IV; 4.0 mg). The prazosin study dose increased forearm blood flow, decreased forearm vascular resistance and venous tone in studies I, III, and IV; these variables were unchanged by prazosin in study II. Despite vasodilator tolerance to the initial daily dosage at 7 months (study II), symptomatic effectiveness and improved cardiac performance were sustained throughout the entire 12 months of chronic prazosin therapy by increasing dosage (study III) and brief interruption of the vasodilator (study IV) (NYHA class IV pre-prazosin symptoms improved to class 2.7 at 3 months, class 2.4 at 6 months, and class 2.5 at 12 months chronic prazosin). This study showed that prazosin vasodilator tolerance occurred in approximately one third of CHF patients after several months of chronic prazosin therapy. More importantly, however, the present investigation demonstrated that chronic prazosin symptomatic efficacy can be maintained in such CHF patients by overcoming tolerance with higher effective prazosin dosage or brief prazosin discontinuation.

Administration, Oral↗
PubMed1981

Efficacy of oral angiotensin-converting enzyme inhibition with captopril therapy in severe chronic normotensive congestive heart failure.

To evaluate the therapeutic efficacy of oral angiotensin-converting inhibition (ACE) with captopril in chronic normotensive congestive heart failure (CHF), acute and cardiocirculatory actions were determined by cardiac catheterization and forearm plethysmography, and ambulatory effects were assessed by echocardiography, nuclear angiography, treadmill exercise, and clinical symptomatology in 10 severe CHF patients. Captopril (90 mg) produced marked (peak 1 hour) and sustained (5 hours) left ventricular filling pressure (23 to 15 mm Hg), systemic vascular resistance decreases, and cardiac index increase (1.99 to 2.41 L/min/m2), while mean blood pressure declined mildly (87 to 80 mm Hg) without heart rate change. Both forearm venous tone and vascular resistance decreased considerably. After 1 week of ambulatory therapy (90 mg three times daily), nuclear angiographic ejection and echocardiogram shortening fractions increased, and exercise duration (341 to 453 sec) and New York Heart Association functional class (3.6 to 2.2) improved. Thus ACE-induced vasodilation by oral captopril improved cardiac performance and clinical status in refractory CHF.

Adult↗
PubMed1981

Effects of diltiazem-induced calcium blockade upon exercise capacity in effort angina due to chronic coronary artery disease.

Few data are available regarding the effects of calcium blockade upon exercise tolerance in patients with stable effort angina due to coronary artery disease (CAD). Therefore we compared the effects of the calcium blocking agent, diltiazem (D), to placebo (P) in 12 patients with chronic effort angina and catheterization documented fixed CAD. The 8-week total protocol consisted of a 1-week baseline period followed by the double-blind randomized crossover alternate 1-week administration of P and D in doses of 120, 180, and 240 mg. Maximal exercise tests (MET) were performed at the end of each 1-week period, while rest radionuclide ventriculography (RVG) was obtained during 240 mg D and corresponding crossover P. Resting heart rate decreased from baseline and initial P at D doses of 60 and 240 mg, but not from P during crossover period. No changes were observed at any dose of D either at rest or during MET in systolic blood pressure or rate . pressure double product. D at 240 mg, but not lower doses, increased MET duration (437 vs 490 seconds, p less than 0.01) and time to angina (383 vs 441 seconds, p less than 0.01). Ejection fraction by RVG was greater with D than P (0.54 vs 0.50, p less than 0.05). Thus these data indicate that calcium blockade with diltiazem provides antianginal efficacy by reducing myocardial oxygen demand, and increases exercise tolerance without depression of myocardial performance in effort angina patients with fixed chronic CAD.

Aged↗
PubMed1981

Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase.

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1/2 hours, disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK therapy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual coronary thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.

Animals↗
PubMed1981

Efficacy of percutaneous transluminal coronary recanalization utilizing streptokinase thrombolysis in patients with acute myocardial infarction.

Since coronary thrombosis is a principal factor in the evolving necrotic process in the majority of patients with acute myocardial infarction (AMI), a prospective study was conducted in 25 AMI patients who underwent expeditious coronary arteriography. Of these patients, 22 with totally occluding thrombus also received early streptokinase (STK) administration. STK was given by intracoronary (20 patients) or systemic (two patients) infusion, 2000 to 50,000 IU/min, to a total dose of 125,000 to 500,000 IU within 10 hours of AMI symptom onset. Eighteen patients had angiographically visualized successful coronary thrombolysis; the shorter the interval between onset of symptoms to treatment, the more rapid was the clot dissolution. Successful thrombolysis occurred concomitantly with readily managed reperfusion ventricular tachyarrhythmias in nearly all patients. In addition, STK recanalization resulted in relief of ongoing chest pain in 10 of 12 patients, 10 of 16 evidenced immediate normalization of hyperacute ST segment abnormalities, and 8 of 14 demonstrated subsequent improvement of angiographically visualized left ventricular (LV) ejection fraction. In the percutaneous transluminal coronary recanalization (PTCR) procedure, the step of using a soft-tipped guide wire itself was transiently useful in only one of seven patients in whom this was attempted; reocclusion took place without added STK therapy. Nitroglycerin (NTG) alone produced only slight distal patency in but 1 of 19 patients with coronary occlusion given the nitrate. Importantly, in 14 control AMI patients receiving conventional treatment without STK, 10 showed angiographically complete occlusion of the coronary artery supplying the infarct region 1 month after infarction, thereby excluding spontaneous clot lysis mimicking STK-PTCR-induced reperfusion. These data support the concept that coronary occlusion by thrombosis is inherently involved with AMI and that rapid PTCR application of intracoronary STK provides potent thrombolysis, superior to that provided by NTG and guide wire passage in reestablishing coronary flow with attendant salvage of jeopardized myocardium and with subsequently improved LV function.

Adult↗
PubMed1981

Hemodynamic actions of prenalterol in severe congestive heart failure due to chronic coronary disease.

To provide improved inotropic agents for enhanced therapy of severe congestive heart failure (CHF), the hemodynamic efficacy of prenalterol (PN), a recently developed cardioselective beta-1 receptor agonist, was evaluated by cardiac catheterization in nine patients with refractory CHF due to chronic coronary disease. PN (4.8 mg intravenously) markedly augmented the cardiac index from 1.9 to 2.6 L/min/m2 (p less than 0.01) and substantially elevated stroke index from 24 to 30 ml/beat/m2 (p less than 0.001). Additionally, PN raised stroke work index 21 to 26 gm.m/m2 (p less than 0.005) and decreased total systemic vascular resistance from 1,702 to 1,260 dynes-sec cm(-5) (p less than 0.001). Concomitantly, heart rate, mean blood pressure, and left ventricular filling pressure were unaltered ( p greater than 0.05). Importantly, the heart rate-systolic blood pressure product was unchanged (p less than 0.05), and precipitation of cardiac dysrhythmias or myocardial ischemia was not observed. Thus PN produced considerable improvement of depressed cardiocirculatory performance without untoward effects and thereby appears a valuable new cardiotonic in the clinical management of severe low output ventricular dysfunction.

Aged↗
PubMed1981

Management of refractory congestive heart failure with prazosin.

The cardiocirculatory actions of prazosin (PZN) orally were evaluated by cardiac catheterization, forearm plethysmography, echocardiography, treadmill exercise, and symptoms in patients with advanced long-standing congestive heart failure (CHF). PZN orally (2 to 7 mg) reduced forearm venous tone and decreased forearm vascular resistance. Concomitantly mean systemic arterial pressure declined, left ventricular filling pressure (LVFP) decreased, and cardiac index (CI) was raised. These effects of a single dose of PZN on LV function were rapid in onset, maximal at 1 hour, and sustained for the entire 6 hours of observation. After 2 weeks of outpatient therapy with 2 to 7 mg PZN four times daily, echographic LV end-diastolic dimension decreased and the duration of treadmill exercise increased. Symptoms (dyspnea, fatigue, angina) were diminished throughout the course of PZN therapy, and New York Heart Association functional class improved for III to II. Thus PZN possesses sustained nitroprusside-like balanced dilator actions on the systemic arterial and venous beds, which are effectively translated into beneficial hemodynamics of augmenting lowered cardiac output and relieving excessive LVFP. Delayed vasodilator tolerance, occurring in 30% of patients, is prevented by prior use of aldosterone antagonists and is easily treated. Subacute hemodynamic suppression of beneficial PZN vasodilator actions is transient and does not preclude successful sustained PZN therapy of severe chronic CHF.

Animals↗