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Biomedical subjects

R W Asinger

Publications and source records attributed to R W Asinger.

At least 37 records · Page 2Linked to original sources
PubMed1993

Echocardiography in the evaluation of cardiac sources of emboli: the role of transthoracic echocardiography.

Cardioembolism is responsible for a significant number of systemic emboli including approximately 15% of all ischemic strokes. Transthoracic echocardiography has contributed to the understanding of cardioembolism and has been used to detect specific and potential cardiac sources of systemic emboli and risk stratify patients with specific clinical findings for subsequent cardiovascular events. Findings from transthoracic echocardiography indicate that stasis is an important prerequisite for intracardiac thrombosis while reversal of stasis and thrombolysis appear operative in embolism of existing thrombus. Transthoracic echocardiography allows a sensitive and specific noninvasive means to detect left ventricular thrombus, valvular vegetation, and intracardiac tumor, lesions that are directly responsible for cardioembolism. Transthoracic echocardiography can also detect lesions that could potentially contribute to cardioembolism but are not specific causes. Examples of these potential lesions include mitral valve prolapse, patent foramen ovale, and interatrial septal aneurysm. Finally, population-based studies and prospective clinical trials have indicated that the results of transthoracic echocardiography have predictive value for subsequent cardiovascular events and hence provide a means for stratification of patients at risk for cardioembolism. The latter is most notable for the group of patients with nonvalvular atrial fibrillation where left ventricular dysfunction and increased left atrial size are independent predictors for subsequent stroke.

Echocardiography↗
PubMed1990

Body fluid spaces and blood pressure in hemodialysis patients during amelioration of anemia with erythropoietin.

Blood pressure (BP) may increase in hemodialysis patients during treatment of anemia with recombinant human erythropoietin (r-HuEPO). Since fluid volume is a determinant of BP in dialysis patients, changes in body fluid spaces during r-HuEPO therapy could affect BP. Thus, 51Cr-labeled red blood cell (RBC) volume, inulin extracellular fluid (ECF) volume, and urea total body water (TBW), as well as cardiac output, plasma renin activity (PRA), and plasma aldosterone concentration were determined postdialysis before and after r-HuEPO therapy in patients in whom changes in BP could be managed by ultrafiltration alone. Eleven patients entered the study: one had a renal transplant and two required addition of antihypertensive drug therapy and were excluded; eight, of whom two required antihypertensive drug therapy following the study, were included in the analyses. Results revealed an increase in predialysis hemoglobin from 67 to 113 g/L (6.7 to 11.3 g/dL) (P = 0.001) during 18 +/- 6 weeks of therapy. Predialysis diastolic BP increased from 80 to 85 mm Hg (P = 0.07), while postdialysis diastolic BP was unchanged at 73 mm Hg. 51Cr-RBC volume increased, from 0.7 to 1.3 L (P = 0.004). ECF tended to decrease, from 13.7 to 10.8 L (P = 0.064), while TBW decreased to a similar extent, but not significantly, 34.3 to 31.2 L (P = 0.16). Postdialysis ECF volume was positively correlated with mean arterial BP at baseline (r = 0.89, P = 0.007) and after therapy (r = 0.74, P = 0.035). However, the regression lines for this relationship were different (P = 0.022) before and after therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Serial changes in left ventricular wall motion by two-dimensional echocardiography following anterior myocardial infarction.

To evaluate the time course of spontaneous changes in wall motion following anterior infarction, we prospectively performed serial apical four-chamber two-dimensional echocardiography on 45 consecutive long-term survivors of initial transmural anterior infarction. Studies were performed on admission (1 +/- 1 days), 1 week after admission (6 +/- 2 days), at discharge (15 +/- 8 days), and at long-term follow-up (235 +/- 186 days). Ventricular size was expressed as end-diastolic area in square centimeters. Wall motion for this tomographic section was evaluated as the percent change in left ventricular area from end diastole to end systole (% LVA). Patients were grouped on the basis of significant differences for %LVA between the first and fourth studies. Group I (n = 14) had improved wall motion (23 +/- 5% to 38 +/- 9%); group II (n = 23) did not change (22 +/- 9% to 23 +/- 11%); and group III (n = 8) had worsened wall motion (28 +/- 6% to 18 +/- 7%). End-diastolic area did not change over the study period for groups I and II but increased significantly for group III (30 +/- 6 to 35 +/- 4 cm2, p less than 0.05). Most of the increase in end-diastolic area for group III was between the third and fourth study. The percent improvement (%IMP) in wall motion for patients in group I who did not have ventricular fibrillation outside the hospital expressed in days (t) following infarction fit an exponential curve (%IMP = 100-100e-(.108t) that predicts that 70% of eventual recovery will occur in the first 15 days post-infarction. We conclude that changes in left ventricular size and wall motion occur following anterior infarction with improvement or worsening occurring spontaneously in some patients. If improvement occurs, it should be evident within 2 weeks of infarction; infarct expansion in this select group of long-term survivors occurred primarily after discharge.

Clinical Enzyme Tests↗
PubMed1988

Early peak of creatine kinase-MB in acute myocardial infarction with a nondiagnostic electrocardiogram.

This study compared the time from the onset of symptoms to the peak of the creatine kinase-myocardial band (CK-MB) in 34 consecutive patients with acute myocardial infarction. Patients were separated into two groups: group 1 (n = 21) had diagnostic (greater than or equal to 0.1 mV) ST segment elevation on the initial ECG, and group 2 (n = 13) did not have diagnostic ST segment elevation on the initial ECG. In group 1 the time to the peak CK-MB was 16.2 +/- 50 hours vs 10.0 +/- 2.0 hours for group 2 (p = 0.0001). Peak CK-MB was 331 +/- 276 IU/L in group 1 vs 81 +/- 54 IU/L in group 2 (p less than 0.005). In group 1 there were 16 patients who subsequently had a Q wave myocardial infarction as opposed to one patient in group 2 (p = 0.0001). Patients who do not have diagnostic ST segment elevation on the initial ECG have an early but low peak of CK-MB and typically have a non-Q wave infarction. These findings are consistent with early spontaneous restoration of blood flow during the infarction process in these patients. This early restoration of blood flow may provide the substrate for the high incidence of recurrent ischemic events noted in patients with non-Q wave myocardial infarction.

Aged↗
PubMed1988

Increasing precordial QRS voltage correlates with improvement in left ventricular function following anterior myocardial infarction.

To evaluate whether changes in QRS voltage reflect changes in left ventricular function after myocardial infarction, 28 patients were studied following anterior myocardial infarction. Two-dimensional echocardiograms and 12-lead electrocardiograms were obtained during the acute phase of the infarction and again after at least 30 days of recovery (mean, 8 +/- 8 months). At follow-up, 11 patients (group A) showed improvement in left ventricular systolic function; 9 had increased net QRS voltage in V1-6 and 8 in V1-4. No improvement in ventricular function was found in 17 patients (group B); 7 had increased QRS voltage in V1-6 (p less than 0.05 vs group A) and only 5 in V1-4 (p less than 0.05 vs group A). For detection of improved left ventricular function, the sensitivity, specificity, and predictive value of the change in net QRS voltage for leads V1-6 was 82%, 59%, and 56% respectively, and for leads V1-4 was 73%, 71%, and 62% respectively. Neither R wave voltage, Q wave voltage, nor the total number of Q waves was reliable for identifying patients with improving left ventricular function. Thus, increasing net QRS voltage in the precordial electrocardiographic leads during long-term follow-up after anterior myocardial infarction correlates with and has a reasonable sensitivity for detection of improvement in left ventricular systolic performance.

Adult↗
PubMed1988

Mesothelioma of the AV node: potential utility of pacing.

Mesothelioma of the atrioventricular node are rare benign tumors with well-described potential for resulting in sudden death. The presentations have varied: the majority of patients have been predominantly female aged 15 to 40, dying suddenly; however, other patients have had documented heart block for many decades and a noncardiac cause of death. A 19-year-old female expired after presenting with ventricular fibrillation and was subsequently discovered to have a mesothelioma involving the AV node. Although high degree heart block is present in many patients, most episodes of sudden death probably are secondary to ventricular tachyarrhythmias. Either form of dysrhythmia may potentially benefit from ventricular pacing.

Adult↗
PubMed1987

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction.

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.

Acute Disease↗
PubMed1987

Two-dimensional echocardiographic identification of complicated aortic root endocarditis: implications for surgery.

Two-dimensional echocardiography successfully displayed the location and extent of aortic root complications, annular abscess or mycotic aneurysm in nine patients with aortic valve endocarditis. Five of the nine patients had prosthetic valve endocarditis and four had native valve endocarditis. The infective process extended into the paravalvular structures, including the interventricular septum (seven patients), right ventricular outflow tract (three patients), interatrial septum (one patient) and anterior mitral valve leaflet (four patients). The amount of aorto-left ventricular discontinuity caused by these complications was quantitated in degrees of annular circumference on the parasternal short axis image and in distance on the parasternal long axis image. The echocardiographic findings were confirmed at surgery and were helpful in the preoperative anticipation of the type of surgical procedure required: aortic valve replacement or composite aortic valve and root replacement. Five patients had prosthetic valve endocarditis with calculated aorto-left ventricular discontinuity of 173 +/- 55 degrees on parasternal short axis images and 1.36 +/- 0.72 cm on parasternal long axis images. Initial surgical repair included three composite aortic root-valve prosthesis implants, one reconstructive procedure with valve replacement and one simple aortic valve replacement. During a follow-up period of 18 months (range 1 to 35), a second reparative procedure was required for only one patient to repair an aortic conduit to coronary artery venous bypass graft. Four patients had native valve endocarditis with calculated aorto-left ventricular discontinuity of 100 +/- 17 degrees on parasternal short axis images and 0.88 +/- 63 cm on parasternal long axis images. Initial surgical repair included two reconstructive procedures with valve replacement and two simple aortic valve replacements. During a follow-up period of 30 months (range 16 to 42), three of these four patients required a second reparative procedure: one each for repair of a paraprosthetic leak, a ventricular septal defect and persistent aorto-left ventricular discontinuity. Two-dimensional echocardiography accurately detected aortic annular abscess and mycotic aneurysm complicating aortic valve endocarditis and the resultant degree of aorto-left ventricular discontinuity. Circumferential aorto-left ventricular discontinuity with these complications is greater for prosthetic than native valve endocarditis and predicts a more extensive surgical repair.(ABSTRACT TRUNCATED AT 400 WORDS)

Abscess↗
PubMed1987

Efficacy, safety, hemodynamic effects, and pharmacokinetics of high-dose moricizine during short- and long-term therapy.

Moricizine, 15 mg/kg, was given to 10 patients with frequent ventricular ectopic depolarizations, eight of whom had previously been treated unsuccessfully with antiarrhythmic drugs. A single-blind inpatient study was followed by therapy for up to 6 months. Two patients developed aggravation of arrhythmia during inpatient therapy. Of the eight patients who completed the inpatient study, seven achieved greater than or equal to 80% suppression of total ventricular ectopic depolarizations (P less than 0.001). During inpatient therapy the mean of the individual patients' suppression of total ventricular ectopic depolarizations was 87.9%, paired ventricular beats 99.3%, nonsustained ventricular tachycardia 99.6%, and premature atrial contractions 89.0%. Suppression was maintained during long-term therapy. The PR interval increased 27% (P less than 0.001), QRS interval increased 10% (P less than 0.0001), QTc increased 1% (P not significant), and JTc decreased 2% (P not significant). Heart rate, blood pressure, and left ventricular performance at rest and exercise were unchanged by moricizine. Moricizine half-life was 9.2 +/- 3.4 hours. Plasma levels of moricizine decreased after 10 days of therapy, suggesting induction of metabolic enzyme systems.

Adult↗
PubMed1986

Two-dimensional echocardiographic detection of left ventricular posterior wall motion abnormalities using an inferior angulation view.

Two-dimensional echocardiography is frequently used to detect left ventricular (LV) wall motion abnormalities. Modification of the apical 4-chamber view by inferior angulation of the transducer provides a superior image for detection of regional wall motion abnormalities of the LV posterior wall. The inferior angulation image was prospectively compared with the standard parasternal short-axis image for detection of posterior LV wall motion abnormalities as defined by contrast left ventriculography in 63 consecutive patients. Posterior wall akinesia was present on the contrast left ventriculogram in 22 of the 63 patients. The parasternal short-axis image was judged technically inadequate for interpretation in 7 patients (11%). The inferior angulation image was technically adequate for interpretation in all patients. The sensitivity, specificity and accuracy of the inferior angulation image for detection of LV posterior wall motion abnormality was 91%, 80% and 84%, respectively, vs 67%, 71% and 70% for the parasternal short-axis image. The differences between the sensitivity, specificity and accuracy for the 2 views were not statistically significant. These observations indicate that the inferior angulation image provides a useful plane for routine echocardiographic analysis of regional LV wall motion either as a primary method to detect posterior wall motion abnormality or as a confirmatory view to document posterior wall motion abnormality.

Adolescent↗
PubMed1986

Two-dimensional echocardiographic identification of left ventricular pseudoaneurysm.

Nine patients with proved left ventricular pseudoaneurysm after transmural myocardial infarction were studied by two-dimensional echocardiography. In all patients two-dimensional echocardiography successfully displayed the pseudoaneurysm. The unique two-dimensional echocardiographic characteristics of pseudoaneurysm include: a sharp discontinuity of the endocardial image at the site of the pseudoaneurysm communication with the left ventricular cavity, and the presence of a relatively narrow orifice in comparison with the maximum diameter of the pseudoaneurysm fundus; visualization of the maximum diameter of the pseudoaneurysm fundus frequently required a slightly different tomographic view than that required for demonstration of the orifice. The distinctive echocardiographic features of pseudoaneurysm in these patients and technical implications for optimal visualization are described. Most of the pseudoaneurysms we encountered and many of those previously described were located posteriorly. We found the use of inferior angulated view modified from the standard apical four-chamber view extremely helpful in detecting the orifice in patients with posterior or posterolateral pseudoaneurysms. We conclude that two-dimensional echocardiography is an important technique for diagnosis of left ventricular pseudoaneurysm.

Aged↗
PubMed1985

Reactive oxygen species may cause myocardial reperfusion injury.

The pathogenic mechanisms responsible for heart damage following temporary coronary artery occlusion are unknown. Some damage may be mediated by a normal cellular enzyme, xanthine dehydrogenase, which converts to xanthine oxidase during myocardial ischemia. Reperfusion, with restoration of oxygen supply, may then lead to formation of superoxide by xanthine oxidase, possibly initiating a cascade of oxidative events. In support of this, reperfusion of transiently ischemic canine myocardium leads to a rapid loss of cellular glutathione and a decrease in catalase activity, both indicative of enhanced generation of activated oxygen. Allopurinol--an inhibitor of xanthine oxidase--ameliorates both biochemical damage and functional deficits ordinarily triggered by ischemia and reperfusion, suggesting one possible mode of pharmacologic intervention following acute myocardial infarction.

Allopurinol↗
PubMed1985

Propranolol antagonism of phenylpropanolamine-induced hypertension.

Phenylpropanolamine (PPA) overdose can cause severe hypertension, intracerebral hemorrhage, and death. We studied the efficacy and safety of propranolol in the treatment of PPA-induced hypertension. Subjects received propranolol either by mouth for 48 hours before PPA or as a rapid intravenous infusion after PPA. PPA, 75 mg alone, increased blood pressure (31 +/- 14 mm Hg systolic, 20 +/- 5 mm Hg diastolic), and propranolol pretreatment antagonized this increase (12 +/- 10 mm Hg systolic, 10 +/- 7 mm Hg diastolic). Intravenous propranolol after PPA also decreased blood pressure. Left ventricular function (assessed by echocardiography) showed that PPA increased the stroke volume 30% (from 62.5 +/- 20.9 to 80.8 +/- 22.4 ml), the ejection fraction 9% (from 64% +/- 10% to 70% +/- 7%), and cardiac output 14% (from 3.6 +/- 0.6 to 4.1 +/- 1.0 L/min). Intravenous propranolol reversed these effects. Systemic vascular resistance was increased by PPA 28% (from 1710 +/- 200 to 2190 +/- 700 dyne X sec/cm5) and was further increased by propranolol 22% (to 2660 +/- 1200 dyne X sec/cm5). We conclude that PPA increases blood pressure by increasing systemic vascular resistance and cardiac output, and that propranolol antagonizes this increase by reversing the effect of PPA on cardiac output. That propranolol antagonizes the pressor effect of PPA is in contrast to the interaction in which propranolol enhances the pressor effect of norepinephrine. This is probably because PPA has less beta 2 activity than does norepinephrine.

Administration, Oral↗