Wolfgang Auffermann
University of California, San Francisco
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Journal of the American College of Cardiology | 1989
Peter T. Buser; Wolfgang Auffermann; William W. Holt; Stephan Wagner; Barbara Kircher; Christopher Wolfe; Charles B. Higgins
Previous reports have validated the accuracy of nuclear magnetic resonance (NMR) imaging for quantitating ventricular volumes and myocardial mass. In this study, a new rapid NMR imaging method, cine NMR imaging, was used to compare left ventricular volumes determined from the transverse plane and short-axis plane in healthy volunteers and patients with dilated cardiomyopathy. With use of the short-axis plane, left ventricular mass at end-systole and end-diastole were determined and left ventricular systolic wall thickening at three different levels was assessed. For validation in the current study, cine NMR imaging and two-dimensional echocardiographic measurements of left ventricular volumes were correlated. Left ventricular volumes of the normal volunteers (end-systolic volume = 34 +/- 3.8 ml, end-diastolic volume = 90.4 +/- 7.2 ml) and patients with cardiomyopathy (end-systolic volume = 173 +/- 28.3 ml, end-diastolic volume = 219.5 +/- 29.6 ml) obtained in the transverse plane were nearly identical to those obtained in the short-axis plane (normal volunteers, end-systolic volume = 30.3 +/- 3.5 ml, end-diastolic volume = 84.7 +/- 7.0 ml and patients with cardiomyopathy, end-systolic volume = 179.1 +/- 27.8 ml, end-diastolic volume = 227 +/- 30.9 ml) and correlated highly (r = 0.91) with volumes obtained by two-dimensional echocardiography. Assessment of left ventricular mass over a broad range using cine NMR imaging in a short-axis plane was identical at end-systole (normal volunteers, 117 +/- 10 g; patients with cardiomyopathy, 202 +/- 20 g) and end-diastole (normal volunteers, 115 +/- 10 g; patients with cardiomyopathy, 194 +/- 21 g).(ABSTRACT TRUNCATED AT 250 WORDS)
American Heart Journal | 1989
Stefan Wagner; Wolfgang Auffermann; Peter T. Buser; Tae H. Lim; Barbara Kircher; Peter Pflugfelder; Charles B. Higgins
Anomalous blood flow caused by valvular regurgitation can be visualized as a narrowly defined area of signal loss in contrast to the high intensity of the blood pool on repetitive gradient refocused magnetic resonance (MRI) (cine MRI) views. In order to assess the accuracy of identification and measurements of the signal void in the evaluation of mitral (MR) and aortic regurgitation (AR), the cine MRI studies of 62 patients with regurgitation and of 20 normal volunteers were retrospectively analyzed in a blinded study of three independent reviewers. Accuracy for detection of MR was greater than 0.96 and for AR was greater than 0.91 for all three reviewers. The total volume of the signal void associated with regurgitation was measured on cine MRI images of 58 patients by two independent observers. The patients were divided into three groups of severity based upon assessment of severity of regurgitation by two-dimensional echocardiography and/or angiography. The total volume of signal loss was 9.0 ml (+/- 0.94 SEE; n = 18) for mild MR, 30.7 ml (+/- 5.3 SEE; n = 11) for moderate MR, and 83.4 ml (+/- 17.4 SEE; n = 5) for severe MR. In patients with AR, the calculated signal void was 27.3 ml (+/- 3.2 SEE; n = 24) in mild, 49.7 ml (+/- 2.9 SEE; n = 7) in moderate, and 75.8 ml (+/- 5.7; n = 6) in severe cases. The differences in the volume of the signal void were significant among the three groups of severity (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Journal of Vascular Surgery | 1988
Pär Olofsson; Wolfgang Auffermann; Charles B. Higgins; Gilberto N. Rabahie; Nuno J. Tavares; Ronald J. Stoney
The accuracy of magnetic resonance imaging (MRI) in the diagnosis of prosthetic aortic graft infection was evaluated in 18 patients with history and findings suggestive of this complication. The prospective interpretation of MRI was compared with surgical findings. Sixteen patients had a graft infection verified at operation. Fourteen patients had infection of the retroperitoneal portion of the graft; two patients had an infection limited to one of the groins; no graft infection was found at surgical exploration in the remaining two patients. Perigraft infection was correctly diagnosed on the basis of MRI findings in 14 of 16 cases; findings were false negative in one case, questionable in another case, and correctly excluded graft infection in two of two cases. MRI also defined the extent of infection in 14 of 16 cases. MRI findings that supported the clinical suspicion of graft infection were perigraft fluid collections remaining more than 3 months after surgery. Furthermore, local inflammation was suggested by an increased signal intensity of adjacent muscle on T2-weighted images in some cases. CT scans were performed in 12 patients; these enabled a correct diagnosis in five and provided indeterminate or false information in seven. These results indicate that MRI is helpful in the diagnosis of aortic graft infection. Furthermore, MRI provides information about the extent of infection crucial for planning therapy.
American Heart Journal | 1989
Wolfgang Auffermann; Thomas Stefenelli; Shao T. Wu; William W. Parmley; Joan Wikman-Coffelt; Dean T. Mason
This study, which was designed to evaluate the effects of positive inotropic agents on intracellular calcium transients ([Ca2+]i), is the first to analyze calcium transients in the whole heart. The positive inotropic agents that augment intracellular cyclic adenosine monophosphate (cAMP) (dibutyryl cAMP, amrinone, and isoproterenol) caused an increase in developed pressure and [Ca2+]i transients and a decrease in diastolic [Ca2+]i. On the other hand, the glycoside digoxin and the alpha-adrenoceptor agents, phenylephrine and dobutamine, also caused an increase in [Ca2+]i transients and developed pressure. However, unlike the agents that increase [cAMP]i, they induced an elevation in diastolic [Ca2+]i. With all the positive inotropic agents, developed pressure increased commensurately with the percentage changes in amplitude of the [Ca2+]i transients.
Journal of Computer Assisted Tomography | 1987
Wolfgang Auffermann; Pär Olofsson; Ronald J. Stoney; Charles B. Higgins
Sixteen patients with a variety of complications of aortic surgery were evaluated with magnetic resonance (MR) imaging. More than one complication occurred in seven patients, resulting in the following types of abnormalities: graft occlusions, two; graft infections; five; pseudoaneurysms or aneurysmal dilatation of graft anastomoses, 10; perigraft hemorrhages, four; and aortoenteric fistulas, two. The MR findings were verified by surgery in 10, by CT in four, and by angiography in 11 patients. The size and extent of pseudoaneurysm or anastomotic dilatation, the presence of thrombus and vessel occlusion, the extent of abscesses, and the effect of pseudoaneurysms and abscesses on adjacent structures were readily demonstrated by MR. The size of the residual lumen in the case of thrombosis could be assessed. Abscesses were identified by their characteristic signal increase with long repetition rates and long echo delays. Magnetic resonance was also able to exclude suspected complications such as perigraft infection, hemorrhage, and graft occlusion in four patients.
American Heart Journal | 1991
Wolfgang Auffermann; Stefan Wagner; William W. Holt; Peter T. Buser; Barbara Kircher; Nelson B. Schiller; Tae Hwan Lim; Christopher L. Wolfe; Charles B. Higgins
The current study used cine magnetic resonance imaging to determine the effect of increasing severity of valvular regurgitation on systolic wall stress and to demonstrate that wall stress was disproportionately increased in relation to the severity of regurgitation in patients with myocardial disease. A total of 39 patients with predominantly mitral (n = 22) or aortic (n = 17) regurgitation with (n = 13) and without (n = 26) myocardial disease and 10 normal volunteers were examined with cine magnetic resonance imaging (MRI) at 1.5 T. Left ventricular (LV) cardiac output (CO) and peak systolic (PS) wall stress (WS) and end-systolic (ES) WS were calculated from blood pressure recordings, carotid pulse tracings, and wall thickness (h) and diameter (D) measurements obtained from cine MRI. Patients were classified into three degrees of severity according to their LV regurgitant volume (RV). Myocardial disease was defined by an ejection fraction (EF) of less than 40%. Mean LV EF was 61 +/- 3% in normal volunteers, 64 +/- 3% in patients with regurgitation, and 25 +/- 2% in patients with myocardial disease. LV CO was directly related to RV in patients without myocardial disease, whereas it was disproportionately low in relation to RV in patients with myocardial disease. PS WS was significantly higher in severe mitral and/or aortic regurgitation compared with moderate, mild, and no mitral and/or aortic regurgitation. Compared with the degree of regurgitation, PS WS was disproportionately higher in patients with myocardial disease. Thus LV CO and WS rise progressively with increasing severity of regurgitation. Disproportionately high systolic WS relative to RV indicates the presence of myocardial disease.(ABSTRACT TRUNCATED AT 250 WORDS)
Basic Research in Cardiology | 1990
Wolfgang Auffermann; Shao Wu; William W. Parmley; Joan Wikman-Coffelt
SummaryGlycolysis is slow in the heart, especially in the cardiomyopathic heart. Glycolysis is partially rate-limited by phosphofructokinase (PFK), an enzymc which is inhibited by calcium (Ca2+)i and hydrogen ions (H+)i and activated by cAMP. (H+)i and (Ca2+)i are augmented in cardiomyopathy. With glucose as the only substrate (NADH)/(NAD) the phosphorylation potential and developed pressure were significantly lower, and concentrations of phosphomonoester sugars and hydrogen ions (H+)i were significantly higher in isolated cardiomyopathic hearts as compared to healthy hamster hearts. Pyruvate lowered diastolic (Ca2+)i in cardiomyopathic hamster hearts. With pyruvate as the substrate (NADH)/(NAD), the phosphorylation potential and developed pressure incrcased significantly and concentrations of phosphomonoester sugars (PME), (H+)i and diastolic (Ca2+)i decreased significantly in myopathic hamster hearts. The results suggest that late heart failure in the myopathic hamster is associated with calcium and/or hydrogen ion-induced inhibition of glycolysis.
American Heart Journal | 1991
Wolfgang Auffermann; Shao T. Wu; Joan Wikman-Coffelt; William W. Parmley
Hamsters were fed 50% alcohol instead of drinking water for up to 42 weeks (average serum alcohol levels were 0.12 +/- 0.06 gm/dl during the 42 weeks). One group of hamsters (28 weeks) was given verapamil 3 days before they were killed. Two groups were withdrawn from alcohol acutely (3 days before they were killed) at 14 and 28 weeks. High-energy phosphate compounds were studied in isolated hearts with 31P-MRS standardized by freeze clamping the tissue. Hemodynamics of the heart were monitored throughout the study. After 7 and 14 weeks of alcohol ingestion, developed pressure and the phosphorylation potential were depressed in the hearts of chronically treated hamsters. At 28 and 42 weeks developed pressure increased but was significantly below baseline values; however, the phosphorylation potential and [pH]i returned to baseline values at 28 and 42 weeks. Throughout the 7 to 42 weeks of alcohol ingestion the alcohol-treated hamsters had a significantly higher end-diastolic pressure as compared with control animals. Withdrawal of alcohol (3 days before the hamsters were killed) reversed the depression of developed pressure and the phosphorylation potential. Acute administration of verapamil (therapeutic dose 3 days before they were killed) to hamsters given alcohol for 28 weeks reversed the depressed hemodynamic values. Overall the data suggest an adaptation of the heart to continuing alcohol consumption, which was related to normalization of the phosphorylation potential and [pH]i and partial alleviation of functional depression.
Cell Calcium | 1990
Wolfgang Auffermann; Shao Wu; William W. Parmley; Joan Wikman-Coffelt
Rat hearts were depleted of Ca2+ (less than 10(-9) M) for 10 min, followed by 15 min of Ca2+-repletion. The calcium paradox injury occurs during Ca2+-repletion, after a period of calcium depletion. The calcium paradox injury was assessed by percent recovery (hemodynamics, [Ca2+]i, and energy levels) during Ca2+-repletion. A decrease in Na+ concentration during Ca2(+)-depletion did not allow for recovery during Ca2(+)-repletion, however 2.5% and 5% ethanol during Ca2(+)-depletion allowed for an approximate 50% recovery during Ca2(+)-repletion. A combination of ethanol (2.5% or 5%) with a low extracellular Na+ concentration (88 mM) allowed for complete recovery. Ethanol prevented a depletion of diastolic [Ca2+]i during Ca2(+)-depletion, and allowed for a return of normal diastolic [Ca2+]i during Ca2(+)-repletion. Ethanol modulates the activity of the Na+/Ca2+ exchanger and protects against the Ca2(+)-paradox injury.
Circulation Research | 1990
Peter T. Buser; Wolfgang Auffermann; Shao Wu; Gaetan Jasmin; William W. Parmley; Joan Wikman-Coffelt
There is controversy as to whether potent inotropic agents are beneficial or detrimental in moderate to severe heart failure. Accordingly, we studied the effects of amrinone, amrinone plus dobutamine, and dobutamine alone on mechanical performance, myocardial oxygen consumption, and high energy phosphate metabolism in different stages of congestive heart failure in the cardiomyopathic Syrian hamster. In hearts with moderate heart failure, administration of amrinone, amrinone plus dobutamine, and dobutamine alone increased developed pressure significantly, whereas the phosphorylation potential increased significantly only with amrinone and amrinone plus dobutamine. In hearts with advanced heart failure, administration of amrinone and amrinone plus dobutamine increased developed pressure significantly, whereas dobutamine alone had no effect. The phosphorylation potential improved significantly only with amrinone. Thus, amrinone improved mechanical performance and mitochondrial activity in both heart failure states. Dobutamine potentiated amrinones beneficial effects in moderate heart failure, but negated the positive inotropic effect of amrinone in advanced heart failure. Therefore, hearts responded differently to potent inotropic agents depending on the severity of heart failure.