Mycotic aneurysm complicating staphylococcal endocarditis.

OBJECTIVE: To emphasize the role of noninvasive diagnostic investigative methods and their importance in early detection of mycotic aneurysm related to staphylococcal endocarditis, and of monitoring therapy or identifying complications. PATIENTS AND METHODS: Two patients with mycotic aneurysm that developed as complications of staphylococcal endocarditis are presented. The first patient had mesenteric artery mycotic aneurysm and presented with sudden rupture one month after initial diagnosis of mitral valve infective endocarditis and completion of a full course of antimicrobial therapy. The second patient had multiple cerebral mycotic microaneurysms and presented with hemorrhagic cerebral embolization from aortic valve infective endocarditis. RESULTS: The first patient died because of ischemic cerebral edema 48 h after rupture of the mesenteric artery mycotic aneurysm and massive hemoperitoneum, which was treated surgically with distal ileal resection and ileostomy. The second patient was alive two years after prolonged antimicrobial therapy and aortic replacement to treat moderate aortic regurgitation and progressive left ventricular enlargement. CONCLUSIONS: Mycotic aneurysm is a rare complication of infective endocarditis but has a high mortality rate because of its early or late potential catastrophic rupture. Diagnosis by noninvasive diagnostic imaging techniques of mycotic aneurysm before rupture would be beneficial for its treatment.

Myocardial functional preservation during ischemia: influence of beta blocking agents.

To determine whether prior acute Beta blockade protects the heart against the deleterious effects of normothermic low flow global ischemia on myocardial function, aortic pressure, developed pressure, dP/dtmax and end diastolic pressure were monitored in isolated perfused rabbit hearts prior to, during and following 30 and 60 min ischemia, during which either Krebs-Henseleit (control) or Beta blocking agents. Bevantolol (cardioselective) or Propranolol (non-selective) were perfused through the heart. Control hearts made ischemic for 30 min and then reperfused had significantly elevated end diastolic (p < .01) and aortic pressures (p < .01) and reduced developed pressure relative to baseline (p < .05). Hearts treated with Bevantolol or Propranolol (3 x 10(-5) m/l) 5 min prior to and during 30 min ischemia recovered preischemic developed pressure and dP/dtmax (p > 0.05), while end diastolic pressure was elevated (p < .01, p < .05 respectively). Aortic pressure was unchanged relative to baseline (p > .05). Comparison of indices from hearts under Beta blockade with controls showed that following 30 min ischemia and recovery, the Bevantolol treated group had reduced aortic pressure (p < .01) and end diastolic pressure (p < .05) and increased percent developed pressure and percent dP/dtmax (p < .001) relative to control. In the propranolol treated group, end diastolic pressure was reduced and percent developed pressure (p < .01) and percent dP/dtmax (p < .001) were increased relative to unblocked hearts. Following 60 min ischemia and 30 min reperfusion, reduction in all functional indices occurred, however dP/dtmax was unchanged from baseline in the Propranolol and Bevantolol treated groups. Comparison between groups showed that the Bevantolol treated group had significantly better dP/dtmax and developed pressure (p < .05), whereas the Propranolol group shows no significant difference from baseline (p > .05) (K-H). We conclude that following short periods of ischemia, Beta blockade protects the heart from deleterious function effects of ischemia but that the protective effect is diminished in Bevantolol relative to Propranolol treatments following prolonged ischemia. The data indicates that the beneficial effects of Beta blockade in reducing ischemic induced damage occurs early during conditions of ischemia such as would be present in the setting of acute myocardial infarction.

Prognostic importance of myocardial ischemia detected by ambulatory monitoring early after acute myocardial infarction.

BACKGROUND: After an acute myocardial infarction, it is important to determine the risk of a subsequent coronary event. We studied the prognostic value of myocardial ischemia detected by ambulatory electrocardiographic (ECG) monitoring in patients who had recently had an acute myocardial infarction. METHODS: Five to seven days after acute myocardial infarction, 406 patients underwent 48-hour ambulatory ECG monitoring, with submaximal exercise testing before discharge and measurement of the left ventricular ejection fraction within 28 days after infarction. Death, nonfatal myocardial infarction, and admission to the hospital because of unstable angina were the principal end points recorded during the one-year follow-up period. RESULTS: The overall incidence of myocardial ischemia detected by ambulatory ECG monitoring was 23.4 percent. The mortality rates at one year were 11.6 percent among the patients with ischemia and 3.9 percent among those without ischemia (P = 0.009); 3.9 percent among the patients with a positive exercise test, 3.0 percent among those with a negative exercise test, and 16.4 percent among those in whom an exercise test was not performed (P < 0.001); and 3.6 percent among the patients with an ejection fraction greater than 50 percent, 3.5 percent among those with an ejection fraction between 35 and 50 percent, and 18.2 percent among those with an ejection fraction below 35 percent (P = 0.001). Using multiple logistic regression, we found that no diagnostic test performed after myocardial infarction provided additional prognostic information beyond that provided by the standard clinical variables used to predict the risk of death. When nonfatal myocardial infarction and admission to the hospital because of unstable angina were also included as outcome variables, ambulatory monitoring for ischemia was the only test that contributed significantly to the model. For the patients with ischemia detected by ambulatory monitoring, as compared with those who did not have evidence of ischemia, the odds ratio was 2.3 (95 percent confidence interval, 1.2 to 4.5) for death or nonfatal myocardial infarction (P = 0.009) and 2.8 (95 percent confidence interval, 1.6 to 4.8) for death, nonfatal myocardial infarction, or admission to the hospital because of unstable angina (P < 0.001). CONCLUSIONS: Myocardial ischemia detected by ambulatory ECG monitoring is common early after acute myocardial infarction and provides prognostic information beyond that available from standard clinical information.

Right ventricular diastolic collapse without hemodynamic compromise in a patient with large, bilateral pleural effusions.

A 22-year-old woman was admitted to the hospital with large bilateral pleural effusions and venous thromboembolism. Echocardiography revealed right ventricular diastolic collapse (RVDC) without physical signs of cardiac tamponade. This echocardiographic abnormality disappeared after thoracentesis. The results of this case report would suggest that pleural effusions were responsible for the echocardiographic finding of RVDC. Presence of RVDC in patients without clinical evidence of cardiac tamponade should alert physicians to look for pleural effusion. Echocardiographic reevaluation after thoracentesis should precede pericardiocentesis.

Left ventricular response in healthy young men during heavy-intensity weight-lifting exercise.

We examined cardiac volumes (using echocardiography), intra-arterial blood pressure (BP), and intrathoracic pressure (ITP) in healthy males performing leg press exercise to failure at 95% of their maximum dynamic strength. Compared with preexercise, during the lifting phase of exercise, end-diastolic volume (EDV; 147 +/- 8 to 103 +/- 7 ml) and end-systolic volume (ESV; 54 +/- 5 to 27 +/- 4 ml) decreased (P < 0.05); heart rate (82 +/- 6 to 143 +/- 5 beats/min), systolic BP (160 +/- 6 to 270 +/- 21 Torr), diastolic BP (91 +/- 2 to 183 +/- 18 Torr), ITP (0.8 +/- 0.8 to 57.8 +/- 24 Torr), and peak systolic BP/ESV (SBP/ESV; 3.0 +/- 0.3 to 11.0 +/- 1.5 Torr/ml) increased (P < 0.05); and stroke volume decreased (94 +/- 3 to 77 +/- 4 ml; P > 0.05). Full knee extension was associated with most values returning to preexercise levels except for ESV (38 +/- 7 ml), heart rate (130 +/- 9 beats/min), and ITP (-12.5 +/- 2.1 Torr). During the lowering phase, significant decreases in EDV to 105 +/- 14 ml and ESV to 27 +/- 7 ml were observed with increases in systolic BP to 207 +/- 23 Torr, diastolic BP to 116 +/- 8 Torr, and SBP/ESV to 10.0 +/- 2.5 Torr/ml. Stroke volume decreased to 78 +/- 9 ml (P > 0.05). Thus rapid changes in cardiac volumes, contractility, and pressure occur during weight lifting that are related to different phases of the lift.

Right atrial myxoma originating from the eustachian valve.

An unusual case of multiple right atrial myxomas arising from the interatrial septum and the Eustachian valve is reported. The literature contains reports of only one other patient with a right atrial myxoma originating from the Eustachian valve.

Effect of high-flux hemodialysis on cardiac structure and function among patients with end-stage renal failure.

The effect of high flux hemodialysis on left ventricular function in ESRD patients was evaluated in a double blind, single cross-over, study comparing conventional to high flux hemodialysis. The subjects were 21 stable chronic hemodialysis patients. Ten were randomly allocated to the conventional-high flux sequence and 11 to the reverse sequence. The conventional membrane was the CD 3,500 or 4,000; the high flux membrane was the Duoflux (Althin Medical Inc., Miami Lakes, Fla.). Both were cellulose acetate and both were sterilized with ethylene oxide. The dialysate bicarbonate and sodium were held constant for the study. The ultrafiltration rates were 3.5-5.0 ml/h/mm Hg transmembrane pressure for the conventional and 15 ml/h/mm for the high flux membrane. The beta-2-microglobulin sieving coefficient was 0 for conventional and 0.27 for the high-flux membrane. The modest improvements in estimates of systolic function suggest a cardiac advantage in high-flux dialysis, the clinical impact of which requires further study.

Preservation techniques for heart transplantation: comparison of hypothermic storage and hypothermic perfusion.

Preservation of the donor heart is an important and controversial subject in heart transplantation. This study compares simple hypothermic storage and hypothermic perfusion in a swine model of heart transplantation (n = 14). The donor hearts of group A (n = 7) were placed in simple hypothermic storage for 5 hours. The donor hearts of group B (n = 7) were placed onto a perfusion apparatus for 5 hours, with pressure maintained at 28 cm of H2O and a myocardial temperature of 8 to 10 degrees C. In both groups the hearts were initially protected with isosmolar potassium cardioplegic solution. The perfusate in group B contained moderate sodium, mannitol, glucose, insulin, and oxygen. The ischemic interval within both groups was 6 hours including orthotopic transplantation. Investigation was conducted at three time periods: prepreservation, postpreservation, and immediately after loading. For both groups there was nonsignificant depression of myocardial function (cardiac index, stroke index, stroke work index, ejection fraction, and wall stress) at the postpreservation period. After volume loading, for the hypothermic perfusion group there was significant improvement of myocardial function (cardiac index, p less than 0.01; stroke index, p less than 0.01) with no significant change in heart rate, systemic vascular resistance, and systolic blood pressure. There was also significant improvement in myocardial performance (p less than 0.05) for the hypothermic perfusion group after volume loading. Ultrastructural changes were minimal for both groups, and there were no major heart transplantation after 6 hours of ischemia; however, hearts retain their contractile capacity better after hypothermic perfusion than after simple hypothermic storage.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of ventricular contractility indexes in the dog with left ventricular dysfunction induced by rapid atrial pacing.

Eight dogs were studied by simultaneous invasive hemodynamic and two-dimensional echocardiographic methods to determine whether left ventricular contractility is altered by 2 weeks of rapid atrial pacing. Additionally, this study evaluated the response of three ventricular contractility indexes to both the pacing intervention and acute load alteration. The indexes compared were ejection fraction, peak systolic pressure to end-systolic volume index ratio (SBP/ESVI) and end-systolic wall stress to end-systolic volume index ratio (ESWS/ESVI). After 2 weeks of pacing at 265 +/- 20 min-1 (mean +/- SD), cardiac index and ejection fraction were reduced to 73 +/- 38 ml/kg per min and 22 +/- 6%, respectively, from 161 +/- 22 and 46 +/- 7 before pacing (both p less than 0.001). Concomitantly, SBP/ESVI and ESWS/ESVI were reduced to 34 +/- 10 mm Hg/ml per kg and 54 +/- 19 g/cm2 per ml per kg, respectively, from 84 +/- 29 and 121 +/- 36 before pacing (both p less than 0.005). There were high correlations for the changes in SBP/ESVI and ejection fraction (r = 0.94, p less than 0.001) and ESWS/ESVI and ejection fraction (r = 0.89, p less than 0.003). Acute afterload alteration with phenylephrine depressed ejection fraction but not SBP/ESVI or ESWS/ESVI. Therefore, this study demonstrates 1) that left ventricular contractility is markedly depressed in the dog by 2 weeks of rapid atrial pacing, and 2) that SBP/ESVI and ESWS/ESVI are superior to ejection fraction as ventricular contractility indexes because these ratios accurately measure contractility changes but are influenced less by after-load conditions.

Improved functional recovery of the atherosclerotic rabbit heart subjected to normothermic global ischemia.

Contractile function before, during and after a period of ischemia was evaluated in perfused hearts from rabbits fed either 2% cholesterol or a control diet for two months. Rabbits were sacrificed and the hearts were perfused by the Langendorff normothermic perfusion technique. After a 30-min baseline period, the hearts were subjected to a 60-min period of low flow ischemia (0.2 mL/min) with Krebs-Henseleit solution containing either 2.5 mM (normocalcemic) or 0.5 mM (hypocalcemic) calcium. Subsequently the hearts were reperfused for 30 mins. No significant differences in baseline contractile function (expressed by developed pressure and dP/dtmax) were observed between hearts from cholesterol-fed and control rabbits. Although, initially the degree of contracture, as measured by an increase in end diastolic pressure from baseline, was less in cholesterol-fed rabbit hearts, this difference did not persist beyond 40 mins of ischemic perfusion. Hypocalcemic ischemic perfusion was associated with a delay in development of contracture relative to normocalcemic perfusion in the hearts from cholesterol-fed rabbits. These results suggest an early resistance to ischemia by hearts from cholesterol-fed rabbits. Upon reperfusion, the hearts from control rabbits exhibited a sudden increase in contracture following ischemic perfusion with 0.5 mM calcium which was not observed in the hearts from rabbits fed a cholesterol diet. There was improved functional recovery and less contracture development post reperfusion in the hearts from cholesterol-fed rabbits, independent of the concentration of calcium used during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular geometry and function in experimental heart failure.

The shape of the left ventricle represents a key element in the adaptation of the heart to a variety of stresses. Therefore, hemodynamic deterioration should be reflected in alterations of shape. To investigate this hypothesis numerical descriptors of shape (single plane, two dimensional shape index, [4 pi (area)/(perimeter)2] and multiplane, three dimensional shape index, [36 pi (volume)2/(surface area)3] were obtained from two dimensional echocardiographic studies in dogs at baseline and then serially during development of early cardiomyopathy. Serial weekly injection of adriamycin (1 mg/kg) in 11 dogs to a cumulative dose of 144 mg/m2 resulted in no significant reduction in ejection fraction, stroke volume or cardiac index (P less than 0.05) but there was demonstrable loss of the ability of the heart to maintain an elliptical configuration during systole. Continuation of treatment to 244 mg/m2 resulted in gradual reduction in ejection fraction, stroke volume and cardiac index. Statistical correlation of the degree of reduction in ejection fraction with change in shape from diastole to systole (change in two and three dimensional shape indices) were -0.803 and -0.855, respectively. These data support the concept that the shape of the left ventricle relates to function, and the inability of the heart to develop an elliptical shape during systole may be an early indicator of impaired function prior to reduction in ejection fraction, stroke volume or cardiac index.

Myocardial protection during ischemia in the isolated perfused rabbit heart.

Although many studies of the protective effects of cardioplegic solutions using hypothermia have been conducted, it is also necessary to examine their protective effects under normothermia as regional increases in myocardial temperature during hypothermic arrest are often reported. For this purpose myocardial protection was investigated in the isolated perfused rabbit heart exposed to 60 minutes of normothermic global ischemia during which Krebs-Henseleit, blood with heparin, Tyers', and St. Thomas' Hospital solutions were infused at 0.2 mL/min. Percent functional recovery dP/dtmax (mm hg/sec) at 5 minutes relative to pre-ischemic values using Tyers' (12 +/- 5)% was significantly less (p less than 0.05) than recovery using Krebs-Henseleit (57 +/- 13)% and St. Thomas' Hospital solution (47 +/- 5)%. Recovery using blood (79 +/- 7)% was significantly better than all other solutions. Following 25 minutes reperfusion, 4/6 hearts perfused with Tyers' experienced left ventricular fibrillation, while recovery of developed pressure with Krebs-Henseleit (74 +/- 5.8)%, St. Thomas' Hospital (66 +/- 3.4)% and blood (98 +/- 2.9)% was again significantly improved relative to Tyers', (p less than 0.05). Time to develop 5 mm contracture during the ischemic period was significantly shorter using Tyers' than with the other solutions. Using these indices of function, whereas Tyers' solution provided poor protection, blood provided excellent protection in rabbit hearts under normothermic conditions.

Adriamycin cardiomyopathy: pathological and membrane functional changes in a canine model with mild impairment of left ventricular function.

Mild impairment of left ventricular function determined echocardiographically was produced in dogs by serial intravenous administration of adriamycin (1 mg/kg/week for 10 weeks). Mild histological changes were observed including vacuolar degeneration but there was a minimal disruption of myocardial architecture (mean severity score 1.4). Ultrastructure of the heart was relatively intact but focal changes included a slight disarray of cellular structure with mitochondrial swelling and distortion, myocytolysis, sarcoplasmic reticular vacuolization, increased glycogen and lipid levels and rounding of nuclei with large condensed nucleoli. Despite involvement of the sarcoplasmic reticulum in damaged myocytes, the transverse-tubules appeared to be normal. It was felt that these changes represent an early stage of adriamycin cardiomyopathy. Ouabain binding was carried out as a test of sarcolemmal integrity. A significant increase in the total number of ouabain binding sites without a change in the dissociation constant was seen. A correlation was observed between the degree of impairment of left ventricular function and the observed increase in ouabain binding. These results support the concept of sarcolemmal membrane alteration as an early mechanism of adriamycin-induced myocardial functional impairment.

Noninvasive determination of valve area in adults with aortic stenosis using Doppler echocardiography.

Doppler ultrasound has been used to determine the pressure gradient P1-P2 across the valve in patients with aortic stenosis (AS), but since the gradient varies over time and may be deceptively low in patients with impaired cardiac output, the key parameter to obtain is the orifice area (A). By calculating stroke volume (SV) from the modal flow velocity [Vmode(t)] over the systolic ejection period (sep) or diastolic filling period (dfp), wherever laminar flow exists in the heart across an area of known diameter D, (pulmonary artery or atrioventricular valves), and by substituting P1-P2 = 4Vmax2, (Vmax = peak velocity in the aortic jet), the Gorlin formula becomes: (Formula: see text) where theta = flow intercept angle at D. This approach was applied in nine adult patients with AS (age 64 +/- 8 years) in whom recent catheterization data was available for comparison. Close correlation was found between the calculated areas: A(Doppler) = 0.82 A(Cath) + 0.17 (r = 0.94, p less than 0.001). Two patients with Doppler gradients of less than 40 mmHg were shown by this Doppler method nevertheless to have severely narrowed orifice areas of less than or equal to 0.78 cm2. Although there is a tendency to overestimate slightly the valve area, Doppler ultrasound assessment using this technique adds valuable noninvasive information concerning the degree of aortic valve disease.

Adriamycin cardiomyopathy: implications of cellular changes in a canine model with mild impairment of left ventricular function.

The present study has examined early cellular effects of chronic adriamycin administration to dogs using a protocol (1 mg/kg/week to a total cumulative dose of 240 mg/m2) producing significant but small reductions in ejection fraction and stroke volume as determined echocardiographically prior to the development of clinical or radiological manifestations of heart failure. At this early phase of cardiomyopathy, significant reduction (P less than 0.05) in sarcoplasmic reticulum Ca2+, K+-ATPase was observed without any change in mitochondrial, lysosomal or sarcolemmal marker enzymes. Myocardial calcium (P less than 0.01) and glutathione (P less than 0.001) levels were increased significantly. Detailed analysis of myocardial phospholipid profiles failed to show any significant differences between control and treated dogs. In contrast, red cell membranes showed increased phosphatidylcholine (PC) and decreased phosphatidylserine (PS) contents, resulting in a significant increase in PC/PS ratio (P less than 0.05). No significant changes were detected in activities of catalase, superoxide dismutase or glutathione peroxidase in erythrocytes or myocardial tissue from control and adriamycin-treated animals. A significant (P less than 0.05) elevation in plasma sialic acid was observed following adriamycin treatment. Our results suggest that early adriamycin-induced damage is unlikely to result from alterations in cellular processes protecting tissues against oxidant injury. Regression analysis indicated that, of the various abnormalities observed, only the elevated myocardial calcium levels and the increases in plasma sialic acid correlated with the degree of myocardial functional impairment. Our findings suggest the presence of sarcolemmal alterations in Ca2+ handling in early adriamycin-induced myocardial injury and indicate that measurement of plasma sialic acid should be further investigated as a possible noninvasive indicator of impending adriamycin cardiotoxicity.

M-mode and two-dimensional echocardiographic abnormalities in systemic lupus erythematosus.

A prospective clinical and echocardiographic study of 47 patients with systemic lupus erythematosus (SLE) and 46 age- and sex-matched controls showed an increased prevalence of echocardiographic abnormalities in the SLE group. Pericardial abnormalities were identified in ten patients with SLE and in no controls. Excluding mitral valve prolapse, valvular abnormalities were identified in ten patients with SLE (21%) and in three controls (7%). In the patients with SLE, abnormalities included mitral valve leaflet thickening in six, aortic valve thickening in five, and mitral annular calcification in two. The presence of valvular abnormalities correlated with duration but not with severity of SLE. The finding of systolic murmurs in 17 of 47 patients with SLE did not correlate with echocardiographic evidence of valvular disease. In six patients with SLE, valvular abnormalities detected by two-dimensional echocardiography were not seen on M-mode echocardiogram.

Abnormalities in heart membranes and myofibrils during bacterial infective cardiomyopathy in the rabbit.

We studied hearts from sham-operated and uninfected catheterized rabbits as well as from rabbits at early and late stages of cardiomyopathy and failure after 3 and 6 days of infection with Streptococcus viridans. No ultrastructural abnormalities or biochemical changes in membrane and myofibrillar activities were seen in 3-day uninfected hearts. In 6-day uninfected hearts there were decreased sarcolemmal M2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding and uptake, and myofibrillar Ca2+-stimulated ATPase as well as increased mitochondrial calcium uptake. Slight ultrastructural changes also were apparent in 6-day uninfected hearts. At both early and late stages of infective cardiomyopathy and failure there were varying degrees of depression in sarcolemmal Mg2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding, calcium uptake and basal ATPase, and myofibrillar Ca2+-stimulated ATPase activities. However, sarcolemmal Ca2+ ATPase and myofibrillar Mg2+ ATPase activities were decreased only after 6 days of infection. Mitochondrial calcium binding and uptake were increased in early stages but decreased in late stages of disease. Furthermore in infected hearts there were defects in mitrochondrial respiration and phosphorylation. Generalized severe myocardial cell damage involving myofibrils, mitochondria, and the sarcotubular system was seen only in late stages of infection. The results demonstrate impairment of different membrane and contractile protein functions as well as ultrastructural abnormalities in bacterial cardiomyopathic hearts which were absent or of lesser magnitude in hearts with only hypertrophy. The findings reported here suggest to use that there is an association between heart failure and changes in function of cellular components during bacterial infective cardiomyopathy.

Alteration in calcium metabolism in cardiac hypertrophy and failure caused by bacterial infection.

Left ventricular hypertrophy was seen in catheterized, uninfected rabbits, whereas contractile failure superimposed upon hypertrophy was observed in catheterized animals after injection with Streptococcus viridans within six days. The infected animals showed marked changes in the ultrastructure of the left heart in comparison to the uninfected rabbits. The levels of calcium and potassium were decreased, whereas sodium was increased in both infected and uninfected hearts; however, magnesium levels did not change in uninfected hearts but were decreased at three days and increased at six days of infection. The microsomal calcium uptake was decreased in six-day uninfected as well as three-and six-day infected hearts. On the other hand, the mitochondrial calcium uptake was increased in six-day uninfected and three-day infected hearts but decreased in six-day infected hearts. The sarcolemmal calcium binding and (Na+,K+)ATPase activities were decreased in six-day uninfected as well as three- and six-day infected hearts. These results dramatic changes in intracellular calcium metabolism in myocardial hypertrophy and failure caused by bacterial infection.

Alterations in myocardial function during bacterial infective cardiomyopathy.

The status of myocardial function in rabbits subjected to cardiac catheterization and infection with Streptococcus viridans was assessed at 3 and 6 days. Sham-operated control animals as well as uninfected catheterized animals were used for comparison. Although left heart hypertrophy and interstitial edema were evident in both uninfected and infected animals, the infected animals exhibited in addition mononuclear cell infiltration and muscle degeneration as well as lung congestion and accumulation of pleural fluid. Both uninfected and infected animals has elevated levels of serum creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase as well as electrocardiographic abnormalities such as increased amplitude of the ORS complex and flattening or inversion of the T wave. Unlike findings in the uninfected animals, the serum calcium, magnesium and sodium levels were slightly but significantly decreased and serum potassium levels were increased in the infected rabbits. Both heart rate and pulse pressure were higher in 6 day uninfected and 3 day infected animals whereas 6 day infected animals showed a decrease in heart rate. In comparison to the sham-operated control rabbits and the uninfected animals, the infected animals exhibited depression in the rates of left ventricular pressure development and relaxation as well as prolongation in time for half relaxation in situ. Relative maximal contractile element velocity extrapolated from intraventricular pressure-velocity curves was decreased by 24, 52 and 76 percent, respectively, of control values in the uninfected hearts and those with 3 and 6 days of infection. The isolated perfused hearts from infected animals also generated less contractile force and showed a decrease in the rates of contraction and relaxation, but half-relaxation time was increased. These results demonstrate myocardial dysfunction during experimental bacterial endocarditis and provide evidence that infective cardiomyopathy is associated with heart failure.