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Biomedical subjects

E L Alderman

Publications and source records attributed to E L Alderman.

At least 127 records · Page 7Linked to original sources
PubMed1978

Effects of alpha adrenergic blockade upon coronary hemodynamics.

The effect of alpha adrenergic block-ade on coronary blood flow regulation at rest was studied in 11 normally innervated patients and 8 cardiac allograft recipients by measuring arterial pressure and coronary sinus blood flow by thermodilution before and after alpha adrenergic blockade with phentolamine. Coronary vascular resistance was calculated by using coronary sinus blood flow and mean arterial pressure, and metabolic demand was estimated by the product of systolic arterial pressure and heart rate. In addition, the coronary sinus blood flow response to tachycardia was examined in 9 innervated patients and 12 denervated patients, with measurements repeated after phentolamine in 8 of the 9 innvervated patients and 6 of the 12 denervated patients. There was a 7.3+/-4.4% increase in coronary sinus blood flow in the innervated patients in response to alpha blockade, whereas the transplanted patients had an 8.2+/-1.8% fall in coronary sinus blood flow, despite equivalent changes in rate pressure product. The innervated patients also demonstrated a significantly greater increase in coronary sinus blood flow than did the transplanted patients during the first 5 s of an abrupt increase in heart rate (26+/-4 vs. 8+/-2.5 ml/min, P <0.001). This early response was blunted after alpha adrenergic blockade. We conclude that there is basal alpha adrenergic tone present on the coronary vasculature in man that is withdrawn by a sudden increase in heart rate.

Adolescent↗
PubMed1978

Six-year clinical and angiographic follow-up of patients with previously documented complete revascularization.

Relatively little information is available concerning the late clinical and angiographic status of patients with initially successful coronary bypass surgery. From 72 patients who had angiography 1 year after bypass surgery, we restudied at 6 years 19 patients with complete revascularization. At 1 year, 14 patients were asymptomatic and five had minimal anginal symptoms. Five years later, eight patients had redeveloped angina, and 11 retained their initial postoperative status. Overall graft patency at 6 years was 86%; 52% of the patients had atherosclerotic progression to > or = 70% luminal narrowing in a major unbypassed vessel or in a major vessel distal to bypass. The patients with unchanged symptoms all had patent grafts, while 11 of the 15 (73%) grafts were patent in patients with symptomatic deterioration (NS). However, progression of coronary disease occurred in seven of eight patients (88%) with worsened symptoms, as opposed to three of 11 patients with unchanged symptoms (P < 0.05). We conclude that late symptomatic deterioration following coronary bypass surgery is common, and that it usually reflects progression of coronary artery disease.

Angina Pectoris↗
PubMed1977

Technetium-99m pyrophosphate myocardial uptake in patients with stable angina pectoris.

99m-technetium (Tc) pyrophosphate myocardial scintigrams of 55 patients with stable angina pectoris were compared with those of 13 normal subjects. The mean scintigraphic score, obtained by averaging the blinded interpretations of four readers scoring on an integral scale from 0 to 4, was significantly higher for the patients with angina than for the control subjects (1.36 compared with 0.48, P less than 0.001). Among the patients with angina, those who had a prior myocardial infarction had a higher mean scintigraphic grade than those without a previous infarction (1.73 versus 1.15, P less than 0.005), and the mean grade in both groups was higher than that of control subjects (P less than 0.001). Radionuclide uptake was predominantly diffuse in the patients with angina pectoris (70%), although in those with greater uptake accumulation tended to be localized. Three of the 68 subjects had high levels of radionuclide uptake but no clinical evidence of acute myocardial injury. This study demonstrates that excess myocardial accumulation of 99m-Tc pyrophosphate can occur in patients with stable angina pectoris.

Angina Pectoris↗
PubMed1977

Ventriculographic and hemodynamic features of mitral regurgitation of cardiomyopathic, rheumatic and nonrheumatic etiology.

Quantitative angiographic findings were reviewed in 40 patients with significant mitral regurgitation classified into three etiologic groups: group I, primary mitral regurgitation (prolapse, ruptured chordae); group II, mixed stenosis and regurgitation of rheumatic origin; and group III, cardiomyopathic mitral regurgitation. For patients in both groups I and II, left ventricular end-diastolic volume was directly related to regurgitant fraction, and ejection fraction was generally well maintained. In contrast, patients in group III had a depressed ejection fraction (less than 0.40) and end-diastolic volume that was disproportionately increased in relation to the degree of regurgitation. Left ventricular end-diastolic pressure was a poor indicator of severity of regurgitation in all patient groups. There was a significant negative correlation between forward cardiac index and regurgitant fraction. There was significant relation, although with considerable variation, between the normalized V wave and regurgitant fraction. The graphs of chamber size, ejection fraction and hemodynamic measures plotted against the severity of regurgitation in different patient groups provide a perspective for interpreting the findings in individual patients.

Angiocardiography↗
PubMed1976

Afterload reduction in the management of postinfarction ventricular septal defect.

The primary goal in the medical management of ventricular septal defect complicating myocardial infarction is to support cardiac function and control symptoms, if possible, for a period of 4 to 6 weeks. If the patient survives this period, surgical correction of the defect is technically easier and safer. In many cases, However, cardiac function is severly compromised, intractable biventricular failure develops,early operation is necessary and the likelihood of successful repair is diminished.

Female↗
PubMed1976

Circulatory response to vasodilator therapy in congestive cardiomyopathy.

Vasodilator therapy has been shown to have beneficial effects in heart failure. In order to evaluate the haemodynamic actions of vasodilator administration in primary congestive cardiomyopathy, sodium nitroprusside was infused intravenously at a rate of 15 to 100 mug/min to 12 patients. Mean arterial pressure fell 15 per cent from 86+/-3-0 to 72+/-2-4 mmHg (11-40 +/- -4 to 9-6 +/- 0-3 kPa), and there was a small but significant decrease in mean heart rate from 96 +/- 4-8 to 90 +/- 4-4 beats/min. These changes were accompanied by a significant decrease in mean pulmonary artery pressure from 40 +/- 2-2 to 26 +/- 2-8 mmHg (5-3 +/- 0-3 kPa to 3-5 +/- 0-4 kPa), mean pulmonary capillary wedge pressure from 25 +/ -2-2 to 16 +/- 2-1 mmHg (3-3 +/- 0-3 to 2-1 +/- 0-3 kPa), and left ventricular end-diastolic pressure from 27 +/- 1-8 to 17 +/- 1-5 mmHg (3-6 +/- 0-3 to 2-3 +/- 0-2 kPa). Cardiac index increased by an average of 48 per cent from 2-1 to 3-1 l/min per m2, and left ventricular stroke work index increased from 18-4 +/- 1-6 to 21-3 +/- 1-9 g m/m2. These results show that pronounced left ventricular dysfunction in patients with congestive cardiomyopathy is improved during vasodilator therapy.

Adult↗
PubMed1976

Evaluation of left ventricular function in patients with aortic regurgitation using afterload stress.

Left ventricular function was assessed in 14 patients with chronic aortic regurgitation by afterload elevation with angiotensin. Seven of 14 patients maintained their resting ejection fraction with angiotensin (group A), while the remaining seven experienced a decline of greater than 0.10 in ejection fraction (group B). Six of seven group A patients showed an appropriate rise in left ventricular stroke work index in response to the angiotensin-induced rise in left ventricular end-diastolic pressure. In contrast, six of seven group B patients showed abnormal, flat, or declining stroke work indices. Included in the seven group B patients were two patients with left ventricular dysfunction secondary to coronary artery disease. The five other group B patients, who did not have coronary diseases, exhibited similar stress-induced ventricular dysfunction, despite the absence of any significant resting hemodynamic differences from patients in group A. These five stress-induced dysfunction patients were distinctive from patients who maintained their ejection fraction level in that the former all had regurgitant fractions of greater than 0.50, whereasl all gruop A patients had regurgitant fractions of less than 0.50. Similarly, these five stress-induced dysfunction patients had significantly larger left ventricular end-diastolic volumes than did the group A patients. These data suggest that patients with pronounced aortic regurgitation measured in terms of regurgitant fraction greater than 0.50 and left ventricular end-diastolic volume of greater than 160 cm3/m2 exhibit impaired ventricular function if appropriately stressed. As most of the patients with stress-induced dysfunction had a normal ejection fraction at rest, it may be that stress-induced dysfunction represents a stage before overt resting dysfunction and cardiac failure.

Adult↗
PubMed1976

Hemodynamic consequences of afterload reduction in patients with chronic aortic regurgitation.

Nitroprusside was used to reduce afterload in 13 patients with isolated, severe aortic regurgitation. The drug significantly lowered mean aortic pressure, pulse pressure, left ventricular end-diastolic pressure and left ventricular volume. Total ventricular, or angiographic, cardiac index was generally unaffected, but forward cardiac index was improved significantly in 8 of 13 patients. Augmentation of forward cardiac index was seen in patients with subnormal resting forward cardiac index, in patients with decidedly elevated end-diastolic pressure, and in those with depressed resting ejection fractions. Regurgitant fraction fell with nitroprusside in six patients and remained unchanged in seven. Total stroke work index was diminished in all patients. These data show that afterload reduction in patients with severe aortic regurgitation may improve hemodynamics by reducing aortic regurgitation or by improving ventricular pump function. The lowered total stroke work, reduced ventricular size and improved forward cardiac index imply that afterload reduction may benefit left ventricular failure and delay progressive ventricular dysfunction in patients with aortic regurgitation.

Adult↗
PubMed1976

Acute hemodynamic interventions shift the diastolic pressure-volume curve in man.

Frame-by-frame analysis of angiograms in 16 patients revealed that hemodynamic interventions are capable of producing substantial shifts in the diastolic pressure-volume curve. Angiotensin raises blood pressure and shifts the entire pressure-volume curve up, and nitroprusside lowers blood pressure and shifts the curve down. Indirect measurements of pleural pressure in seven patients (via esophageal pressure) showed that pleural pressure changes were too small to account for these shifts. Analyzing our results in terms of a theoretical pressure-volume equation previously validated in dog studies did not show the observed shifts to be the product of acute changes in the elasticity of the myocardium itself. This same analysis suggested that indirect changes in the external mechanical constraints acting on the left ventricle such as the right ventricular pressure, the pericardium, and perhaps viscoelastic effects related to changes in filling rate account for the pressure-volume curve shifts with intervention. The fact that one cannot in general relate a specific volume to a given pressure in the face of hemodynamic interventions calls into question the use of end-diastolic pressure interchangeably with end-diastolic fiber length when interpreting systolic events in terms of the Frank-Starling mechanism.

Adult↗
PubMed1976

Treatment of recurrent symptomatic ventricular tachycardia.

Eleven consecutive patients with recurrent ventricular arrhythmias were treated by an aggressive protocol and followed up prospectively. Arrhythmias, symptoms, and cardiac lesions were defined. Antiarrhythmic drugs were given on schedule, with blood levels determining dose; success or failure was defined by elimination or recurrence of symptomatic arrhythmias. When drug therapy failed, left ventricular aneurysmectomy was done when appropriate. Recurrent ventricular tachycardia was most frequently responsible for symptoms; coronary artery disease was the most frequent underlying disease. Symptomatic arrhythmias were eliminated in 8 of 11 patients (5 with drugs and 3 with aneurysmectomies), with a 16.5-month symptom-free average follow-up. An average of 2.9 therapeutic trials per patient was needed to control symptomatic arrhythmias. The average time from entry into the study until the start of ultimately effective therapy was 18 days. Therapy that eliminated symptoms did not eliminate all premature ventricular contractions, and occasionally even brief asymptomatic episodes of ventricular tachycardia persisted. Recurrent symptomatic ventricular arrhythmias can be controlled in many patients by rigorous application of current therapies.

Adult↗