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Biomedical subjects

A N DeMaria

Publications and source records attributed to A N DeMaria.

At least 181 records · Page 10Linked to original sources

Multiclinic controlled trial of diltiazem for Prinzmetal's angina.

To assess the efficacy of a new calcium entry blocker, diltiazem (Cardizem), for prophylaxis of Prinzmetal's angina, 48 patients were studied in randomized, multiple crossover multiclinic study (2 weeks single-blind, 8 weeks double-blind). Diltiazem dosage in one crossover phase was 120 mg per day; in the other, 240 mg per day. Therapeutic response was measured by patients' diary records of angina frequency and nitroglycerin tablet consumption. Treatment with 120 mg of diltiazem per day reduced angina by 41 percent from the entry placebo period and 20 percent from the paired placebo period (p less than 0.005). Treatment with 240 mg of diltiazem per day reduced angina frequency by 68 percent from the entry placebo period and 43 percent from the paired placebo period (p less than 0.01). There were similar reductions in nitroglycerin consumption. Adverse experiences that may have been related to the medication were noted in only 5 percent of patients. There were no alterations in blood pressure or heart rate. The PR interval increased 3 percent at the 240 mg dosage level. We conclude that diltiazem is an effective and safe agent for control of symptoms of Prinzmetal's angina.

Adult↗

Beneficial effects of nitroprusside administration on left ventricular dysfunction and myocardial ischemia in severe aortic stenosis.

Although surgical therapy is effective for reducing excessive left ventricular (LV) afterload in valvular aortic stenosis (AS), salutary short-term medical treatment has been lacking. Since we have shown LV systolic pressure (SP) is altered concordant with arterial SP in AS by vasopressors, the present study evaluated efficacy of nitroprusside (NP) on LV function, energetics, and perfusion in 15 severe AS patients. NP infusion (average 33 micron/min) proved beneficial in each: LVSP 192 mm Hg was reduced to 164; arterial SP decrement equaled LVSP change; LV end-diastolic pressure 19 mm Hg declined to 10: cardiac index (2.73 L/min/m2) and heart rate were unaltered; total systemic vascular resistance 1433 dsc-5 decreased to 1201; elevated LV stroke work index 92 gm.m/m2 was diminished to 74. Simultaneously, LV O2 consumption fell, LV diastolic flow was unchanged, while subendocardial perfusion increased. Thus cautious NP therapy with careful monitoring provided marked reduction of LV affected and improved LV function, energetics, and coronary flow distribution.

Aged↗

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↗

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↗

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↗

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↗

Short- and long-term therapy of mild essential hypertension with timolol.

The short and long-term antihypertensive action of timolol, a beta blocker, was assessed in 36 mild hypertensives in a 32-wk, double-blind, placebo-controlled study followed by an additional 96 wk of timolol in 17 responders. Diastolic blood pressure (DBP) and heart rate (HR) declined during the first phase from 103 to 93 mm Hg and from 73 to 61 bpm (P less than 0.01) but there was long-term timolol subjects (DBP 89 mm Hg at 32 wk and 88 mm Hg at 96 wk [NS] and HR 62 and 65 bpm [NS]). Although stimulated plasma renin activity in the entire group decreased from 1.08 to 0.28 ng/ml/hr (P less than 0.001), blood pressure reduction did not correlate with this decline (r = 0.29) or with serum timolol level (r = 0.29). In 20 patients who underwent treadmill was not altered. Thus, timolol is effective in reducing mild high blood pressure during short-term therapy and in maintaining this effect over the long term in responsive subjects. It is therefore potentially useful in chronic essential hypertension.

Adult↗

Hemodynamic effects of morphine and nalbuphine in acute myocardial infarction.

Hemodynamic effects of morphine and the new narcotic analgesic, nalbuphine, were compared in a randomized, double-blind study in 15 patients with acute myocardial infarction (11 men and four women, average age 56.2 yr) and normal group mean hemodynamic function. During a 1-hr evaluation the hemodynamic effects were small but there were changes in several parameters. Morphine reduced heart rate (78 to 72 bpm, p less than 0.01) and diastolic and mean arterial pressures (69 to 64 mm Hg, p less than 0.05; and 91 to 84 mm Hg, p less than 0.05); nalbuphine was associated with a decrease in heart rate (82 to 72 bpm, p less than 0.01), decrease in cardiac index, which remained within the normal range (3.16 to 2.75 l/min/m(2), p less than 0.01), and an increase in systemic vascular resistance (1,204 to 1,461 dynes . sec . cm(-5), p less than 0.05). Neither drug altered systolic arterial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, stroke index, stroke work index, or pulmonary vascular resistance. Echocardiographic assessment revealed diminution of left ventricular mean velocity of circumferential fiber shortening after nalbuphine (1.26 to 1.08 circ/sec, p less than 0.05). Both drugs induced small reductions in respiratory rate and arterial pH and increases in PAO2. There were no changes in PaO2. Because of the absence of clinically important deleterious effects on cardiac pump function, nalbuphine merits further investigation as an analgesic in acute myocardial infarction.

Adult↗

Cross-sectional echocardiography: physical principles, anatomic planes, limitations and pitfalls.

Although M mode echocardiography has achieved a prominent role in the diagnosis and management of patients with cardiovascular disease, the limited area of view afforded by M mode techniques has restricted the application of ultrasound in many areas. The development of two dimensional echocardiography has obviated many of the limitations inherent in the narrow view of the M mode technique. It has enabled imaging of the heart from additional transducer locations, permitted determination of shape and anatomy and provided the ability to determine motion along two axes. Several types of two dimensional echocardiographs have been developed, and each type offers both advantages and disadvantages. Although two dimensional echocardiography has provided a larger area of view with ultrasound, it has also introduced new limitations including a larger and bulkier transducer, a much reduced sampling rate and a difficult display medium (videotape). In addition, new considerations regarding ultrasonic resolution have been raised. Two dimensional techniques have resulted in new pitfalls in ultrasonic diagnosis related to instrument artifacts as well as to performance and interpretation of the examination. The spurious appearance of cardiac masses because of these ultrasonic artifacts represents a particularly prominent diagnostic pitfall that must be avoided in daily practice. It is anticipated that the new wider field of view provided by two dimensional echocardiography combined with a standard high resolution capability of ultrasound (2 to 4 mm) will result in an increasingly large role for echocardiography in the management of patients with heart disease.

Cardiovascular Diseases↗

Value and limitations of two dimensional echocardiography in assessment of cardiomyopathy.

Primary myocardial diseases have traditionally been classified into congestive, hypertrophic and restrictive varieties. M mode echocardiography has proved extremely valuable in distinguishing congestive cardiomyopathy with major ventricular dilation and poor contractile performance from hypertrophic cardiomyopathy with predominant left ventricular hypertrophy (septum greater than posterior wall) and normal pump performance, and restrictive disorders with symmetric ventricular wall thickening and normal or diminished contractile function. The contributions of two dimensional echocardiography to the evaluation of patients with congestive or restrictive cardiomyopathy have been limited to certain specific situations, such as the recognition of left ventricular mural thrombi. Twenty-five patients with hypertrophic cardiomyopathy were studied to assess two dimensional echocardiography in the evaluation of patients with this disorder. Two dimensional echocardiography indicated that hypertrophy of the interventricular septum is not uniform from apex to base in all patients but may be greatest in the apical, mid or basal third. In addition, the anterior free wall of the left ventricle was involved in the hypertrophic process in approximately 50 percent of patients. Two dimensional echocardiography documented that the location of systolic anterior motion of the mitral valve in patients with hypertrophic cardiomyopathy is most often at the junction of the mitral valve leaflets and chordae tendineae, although the chordae themselves and even th papillary muscles may be involved in this movement. The heterogeneity of these characteristics may enable patients with hypertrophic cardiomyopathy to be classified into subsets of patients in whom meaningful therapeutic and prognostic implications may be derived. Finally, data derived from two dimensional echocardiography have shown that, although the left ventricle in hypertrophic cardiomyopathy conforms in some degree to the configuration of a catenoid, this geometric conformation is unlikely to account for the genesis of this order.

Cardiomegaly↗

Imaging procedures in the detection of cardiac tumors, with emphasis on echocardiography: a review.

Although cardiac tumors are relatively rare, their diagnosis is important because successful treatment is usually feasible if the diagnosis is made preoperatively. An analysis of 219 reports of cardiac tumors described in the English literature from 1972 through 1977 demonstrated the predominance of benign tumors, in particular myxoma, which is in agreement with past reviews. The methods of diagnosis employed included plain chest films, echocardiography, cardiac catheterization, angiocardiography, and cardiac scintigraphy. Conventional x-ray examination of the chest was abnormal in 83% of cardiac tumors but non-specific and should lead to further evaluation, first by echocardiography. Echocardiography, the most efficient diagnostic procedure for screening possible cardiac tumors, was abnormal in 94% of the cases. Cardiac catheterization was abnormal in 80% of cardiac tumors while definitive detection was made by angiocardiography in 94% of the cases. Cardiac scintigraphy has had limited use in the diagnosis of cardiac tumors, but has been diagnostic in 100% of the cases in a small series of myxomas.

Adult↗

Evaluation of transluminal angioplasty of chronic coronary artery stenosis. Value and limitations assessed in fresh human cadaver hearts.

The possibility of increasing reduced blood flow in atherosclerotic coronary obstruction by catheter balloon dilatation offers a nonsurgical approach to relieve clinical coronary stenosis. To assess the ability of effectively dilating such diseased vessels by transluminal angioplasty, we used the Grüntzig balloon-tipped catheter in 12 fresh human cadaver hearts in which the intervention was performed in 21 noncalcified stenotic areas, including each of the three major coronary arteries. Quantitative coronary arteriography documented decreased obstruction of each lesion; luminal diameter increased 58% (1.9 +/- 0.2 mm to 2.8 +/- 0.3; p less than 0.001) and luminal diameter relative to the most proximal normal coronary segment diminished 61% (46 +/- 4% to 18 +/- 3%; p less than 0.001). Angioplasty was most successfully applied in proximal, discrete, noncalcified lesions of the right and left anterior descending coronaries; calcified, tortuous, middle and distal lesions and the left circumflex coronary were entered with difficulty or unapproachable. Histologic examination revealed microanatomic changes, most often endothelial disruption and atheroma compression, but no serious vascular tears. Dilatation beyond normal coronary diameter caused vessel rupture. This study extends elucidation of the value and limitations of percutaneous transluminal angioplasty in the clinical use of this technique in selected patients for relieving coronary obstruction without surgery.

Arterial Occlusive Diseases↗