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M L Hess

Publications and source records attributed to M L Hess.

157 records · Page 9Linked to original sources
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Glucose, insulin, potassium protection during the course of hypothermic global ischemia and reperfusion: a new proposed mechanism by the scavenging of free radicals.

Glucose, insulin, potassium (GIK: 300 g glucose + 50 U insulin + 80 mEq KC1/L) was administered to anesthetized dogs as a 30-ml bolus followed by 1.5 ml/kg/h for 2 h. Five populations were studied: control (C, n = 6); 60 min hypothermic arrest both without (I, n = 6) and with pretreatment (I + GIK, n = 6); 60 min hypothermic arrest followed by reperfusion without (R, n = 6) and with pretreatment (R + GIK, n = 6). Glycogen content declined during the ischemic and reperfusion periods whether or not GIK pretreatment was utilized. Glycogen values did not differ significantly among the four groups. GIK pretreatment significantly protected sarcoplasmic reticulum (SR) calcium uptake rates. SR Ca2+ + Mg2+ adenosine triphosphatase (ATPase) activity was unaffected in the I group, depressed in the R group, but protected by GIK pretreatment. Myofibrillar pCa-ATPase activity was significantly depressed in the I group and unaffected by GIK pretreatment. In the R + GIK group, myofibrillar pCa-ATPase activity was identical to controls at all calcium concentrations except for Vmax. In vitro, generation of the superoxide anion by a xanthine-xanthine oxidase system at pH 7.0 significantly depressed both SR calcium uptake and ATPase activity, and this depression was partially reversible by glucose. Generation of the hydroxyl free radical and pH 6.4 significantly depressed calcium uptake but not ATPase activity, and this depression was reversible with glucose + superoxide dismutase. GIK pretreatment exerts a protective effect on the excitation-contraction coupling system during hypothermic global ischemia and reperfusion. Glycogen augmentation after short-term GIK infusion was not significantly different. It is hypothesized that an additional mechanism by which GIK may protect subcellular function is by serving as a scavenger of free radicals generated during the ischemic/reperfusion process.

Adenosine Triphosphatases↗
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Hypercholesterolemia in long-term survivors of heart transplantation: an early marker of accelerated coronary artery disease.

Coronary artery disease remains a significant long-term problem for survival after heart transplantation. Hyperlipidemia is a known risk factor for coronary artery disease in the general population, but the role of hyperlipidemia in cardiac allograft recipients has not been elucidated. To study this problem, we retrospectively reviewed 38 heart transplant recipients who survived more than 3 years after surgery and looked at age, development of diabetes, drug protocol, and development of hypercholesterolemia for a possible correlative or predictive value to the development of early coronary artery disease after heart transplantation. Eleven patients were identified as having coronary disease by the third year after transplantation. High-risk cholesterol values (in milligrams per deciliter) at 6 months after heart transplantation were defined as follows: for ages 10 to 20, 190; 20 to 30, 220; 30 to 40, 240; 40+, 260. We found a strong predictive value with high-risk lipid profiles (p less than 0.01) for the development of coronary artery disease by the third year. No significance was found for a low-risk value, the development of diabetes, or hypertension. All patients below the age of 20 years had coronary artery disease by the third year after transplantation. We conclude that a high-risk cholesterol value at 6 months after transplantation is a strong predictor for development of accelerated coronary artery disease and early graft failure. This has major implications for management of hyperlipidemia in the cardiac allograft recipient.

Adult↗
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Results of heart transplantation for active lymphocytic myocarditis.

To determine whether the heart-specific immunoreactivity associated with active myocarditis affects outcome after heart transplantation, we retrospectively analyzed the outcome of 12 patients with active lymphocytic myocarditis in their explanted native hearts identified by the Registry of the International Society for Heart Transplantation. The patients were 38 +/- 10 years of age and predominantly female (75%). In nine patients (75%), endomyocardial biopsy showed active myocarditis before transplant; eight of these patients also received immunosuppression before transplant. Recipient hemodynamic study before transplantation demonstrated an ejection fraction of 0.18 +/- 0.06, cardiac index of 1.7 +/- 0.4 L/min/m2, pulmonary artery pressure of 41 +/- 6/23 +/- 6 mm Hg, and mean pulmonary capillary wedge pressure of 30 +/- 5 mm Hg. Left ventricular end-diastolic dimension by echocardiography was 6.0 +/- 1.4 cm. Four of the patients were dependent on intravenous inotropes, and six required mechanical assistance. Over a 36-month follow-up period, 2.9 +/- 2.4 episodes of rejection occurred per patient. Sixty percent of the first episodes occurred within 2 weeks of transplantation. These patients experienced a 2.2 +/- 1.1-fold increase in rejection compared with institutional average rejection rates. Survival was significantly shorter than that of age-matched or female control subjects. This study is limited by its retrospective nature and the unusual pretransplant characteristics of the subjects. It indicates that active myocarditis may predispose patients to early severe rejection and a high mortality rate after heart transplantation.

Adult↗
PubMedDate not supplied

Hyperlipidemia after clinical heart transplantation.

Accelerated coronary atherosclerosis is a major cause of morbidity and death in the cardiac transplant recipient. Hypercholesterolemia has been implicated as a contributing risk factor. Because of this we reviewed lipoprotein profiles from transplant recipients from 1968 to 1986 in an attempt to identify the risk factors for the development of lipid disorders after transplantation. Patients were divided into three groups based on their immunosuppressive protocols. Group 1 consisted of 10 patients receiving azathioprine and prednisone. Group 2 consisted of 24 patients receiving cyclosporine and prednisone with or without azathioprine. Group 3 consisted of 18 patients receiving cyclosporine and azathioprine without prednisone. Total cholesterol levels at 1 year were highest in group 2 (266 mg/dl versus 236 mg/dl for group 1 [p = 0.16] and 223 mg/dl for group 3 [p = 0.005]). High-density lipoprotein cholesterol levels were lowest in group 3 (38 mg/dl versus 51 mg/dl for group 1 [p = 0.025] and 54 mg/dl for group 2 [p = 0.0001]). Subgroup analysis with multivariate and univariate analysis found that prednisone and preoperative coronary artery disease are the major contributors to the posttransplant lipid abnormalities.

Adult↗
PubMedDate not supplied

Contrast injection bradycardia during coronary angiography: effects in the denervated human heart.

To assess the contribution of cardiac innervation toward understanding the mechanisms of bradycardia during contrast coronary angiography, heart rate (HR) responses in eight patients after heart transplantation were compared with 10 normal patients (control), 10 patients with coronary artery disease (CAD) and normal ventricular function, and 10 patients with congestive cardiomyopathy and normal coronary arteries. The longest P-P interval was measured beat to beat before (HR 1) and after (HR 2) coronary angiography. The coronary vessel perfusing the sinus node did not influence HR 2 responses within each group. HR 1 was significantly different from HR 2 (p less than 0.05) in the control and CAD groups but was not different in the transplant and cardiomyopathy groups. Compared with the control group, the percent decrease in HR was significantly less in transplant patients than in patients with cardiomyopathy. Thus contrast injection bradycardia is absent in denervated patients after heart transplant, and this response is markedly blunted in cardiomyopathy patients who are known to have diminished vasodepressor reflexes. These findings suggest that the bradycardia response is probably a neurally mediated phenomenon.

Adult↗
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Expectations and limitations of endomyocardial biopsy.

Endomyocardial biopsy represents an attempt at applying tissue examination to the diagnosis of primary myocardial disease. The right ventricular septum is biopsied from either the internal jugular or femoral venous approach. Left ventricular endomyocardial biopsy has not gained widespread acceptance in North America. A complication rate of 1-4% has been reported. Clinical indications for endomyocardial biopsy include acute cardiac allograft rejection, adriamycin cardiotoxicity and the differentiation of restrictive myopathy from constrictive pericardial disease. The biopsy of patients with idiopathic dilated congestive myopathy to find a treatable form of myocarditis remains controversial and principally a research tool. Only 5-25% of patients with dilated cardiomyopathy are found to have myocarditis and immunosuppressive therapy in these patients has yet to be proven beneficial.

Biopsy↗
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Left ventricular function of heart allografts during acute rejection: an echocardiographic assessment.

Left ventricular function was evaluated in nine patients during biopsy proven acute rejection of heart allografts using computer-assisted analysis of echocardiograms. The results were compared with data obtained during their non-rejection state and with data obtained from 10 normal subjects. Left ventricular dimensions and parameters of diastolic and systolic function of non-rejecting hearts were similar to those of normals. Acute rejection was associated with increased left ventricular mural thickness and mass, and abnormal diastolic function characterized by a prolongation of the rapid filling period from 155 msec +/- 14 msec to 183 msec +/- 16 msec (p less than 0.05, mean +/- SE), and decreased normalized peak rates of left ventricular lengthening (from 5.3 sec-1 +/- 0.8 sec-1 to 3.9 sec-1 +/- 0.4 sec-1, less than 0.05) and posterior wall thinning (from 7.4 sec-1 +/- 1.0 sec-1 to 3.8 sec-1 +/- 0.6 sec-1, p less than 0.05). Parameters of systolic function as defined by fractional shortening, peak normalized rates of left ventricular shortening and posterior wall thinning were not altered by acute rejection. We conclude that the left ventricular function of non-rejecting hearts is similar to that of normals; however, acute rejection is associated with abnormal left ventricular diastolic dynamics without adverse effect on systolic function.

Adult↗