[Traumatic Right Atrial Rupture with Left Hemothorax but without Hemopericardium:Report of a Case].

Traumatic cardiac rupture is mostly accompanied by tamponade and/or hemopericardium. We experienced a rare case of traumatic right atrial rupture with left hemothorax, but without hemopericardium. A 36-year-old male had a traffic accident, and was transported to our hospital. He was in a state of shock caused by massive hemothorax. He underwent emergency operation through median sternotomy. No blood was seen in the pericardium nor injury of any major vessels or lungs. When the heart was exposed, massive bleeding occurred. A tear of 30 mm in length was found in the right atrium at the junction of the superior vena cava. The tear was repaired under cardiopulumonary bypass. Even after surgery, however, he remained unconscious.

Infective Endocarditis with Intermittent Atrioventricular Block and Pseudoaneurysm of the Mitral-aortic Intervalvular Fibrosa in a Patient with Severe Aortic Stenosis.

Atrioventricular (AV) block and pseudoaneurysm of the mitral-aortic intervalvular fibrosa (P-MAIVF) are rare complications of infective endocarditis (IE). A 72-year-old man with severe aortic stenosis was hospitalized due to IE. After admission, intermittent AV block and P-MAIVF were noted. Interestingly, an accelerated junctional rhythm was observed during the process of AV block resolution. Elective surgery, which included patch closure of the fistula and replacement of the aortic valve, was successfully performed. The patient has remained in good condition without the recurrence of AV block. This case report describes a rare comorbidity of AV block and P-MAIVF in a patient with aortic valve IE.

Two cases of colonic necrosis following aortoiliac surgery due to coronary-induced cardiogenic shock.

We report two cases of abdominal aortic aneurysm in which the patent inferior mesenteric arteries were ligated. The patient in Case 1, with occlusion of the right coronary artery, developed sudden bradycardia during surgery, resulting in cardiac arrest. The patient was successfully resuscitated and the operation was completed. In Case 2, acute thrombotic obstruction occurred postoperatively in the stent previously implanted in the left anterior descending coronary artery. Although the thrombus was removed by aspiration, hypotension was sustained. In both cases, colonic necrosis extending from the descending colon to the rectum developed following cardiogenic shock. The affected portion of the colon was resected and a colostomy was constructed. The incidence of coronary arterial disease is high in patients with abdominal aortic aneurysm. The occurrence of cardiac complications is not rare, and may result in catastrophic consequences. Therefore the inferior mesenteric artery should be reimplanted, especially in patients with concomitant heart disease.

Remodeling of the chronic severely failing ischemic sheep heart after coronary microembolization: functional, energetic, structural, and cellular responses.

The mandatory use of pharmacotherapy in human heart failure (HF) impedes further study of natural history and remodeling mechanisms. We created a sheep model of chronic, severe, ischemic HF [left ventricular (LV) ejection fraction (LVEF) <35% stable over 4 wk] by selective coronary microembolization under general anesthesia and followed hemodynamic, energetic, neurohumoral, structural, and cellular responses over 6 mo. Thirty-eight sheep were induced into HF (58% success), with 23 sheep followed for 6 mo (21 sheep with sufficient data for analysis) after the LVEF stabilized (median of 3 embolizations). Early doubling of LV end-diastolic pressure persisted, as did increases in LV end-diastolic volume, LV wall stress, and LV wall thinning. Contractile impairment (LV end-systolic elastance, LV preload recruitable stroke work, and dobutamine-responsive contractile reserve) and diastolic dysfunction also remained stable. Cardiac mechanical energy efficiency did not recover. Plasma atrial natriuretic peptide levels remained elevated, but rises in plasma aldosterone and renin activity were transient. Collagen content increased 170%, the type I-to-III phenotype ratio doubled in the LV, but right ventricular collagen remained unaltered. Fas ligand cytokine levels correlated with expression of both caspase-3 and -2, suggesting a link in the apoptotic "death cascade." Caspase-3 activity also bore a close relationship to LV meridional wall stress calculated from echocardiographic and intraventricular pressure measurements. We concluded that the stability of chronic untreated severe ischemic HF depends on the recruitment of myocardial remodeling mechanisms that involve an interaction among hemodynamic load, contractile efficiency/energetics, neurohumoral activation, response of the extracellular matrix, wall stress, and the myocyte apoptotic pathway.

Glucose-insulin-potassium solution improves left ventricular energetics in chronic ovine diabetes.

BACKGROUND: Therapeutic modulation of myocardial metabolism improves outcomes in diabetic patients following myocardial infarction and coronary artery surgery. However, the mechanism of this beneficial effect has not been fully elucidated. This study evaluated the effect of glucose-insulin-potassium solution (GIK) on left ventricular (LV) energetics and oxygen utilization efficiency in a chronic ovine model of diabetes. METHODS: Diabetes was induced in sheep with streptozotocin. Experiments were performed following 12 months untreated diabetes (n = 6) and in controls (n = 6). Open-chest anesthetized sheep were instrumented to determine the LV pressure-volume relationship, oxygen consumption, and free fatty acid uptake. Glucose-insulin-potassium was infused at 1.5 mL x kg(-1) x h(-1) for 60 minutes and assessment repeated. RESULTS: Glucose-insulin-potassium decreased LV free fatty acid uptake in control: 0.090 +/- 0.047 microg/beat/100 g to 0.024 +/- 0.022 microg/beat/100 g, p = 0.02 and diabetes: 0.33 +/- 0.32 microg/beat/100 g to 0.11 +/- 0.13 microg/beat/100 g, p = 0.04. Similarly, GIK decreased unloaded left ventricular oxygen consumption (LVVO(2)) in both control (0.42 +/- 0.05 to 0.37 +/- 0.13J/beat/100 g, p < 0.001) and diabetic sheep (0.40 +/- 0.24 to 0.23 +/- 0.23J/beat/100 g, p < 0.001). The slope of the LVVO(2)-pressure-volume area relation (contractile efficiency) was unchanged in either group. Glucose-insulin-potassium improved LV contractility 58% +/- 37% (p = 0.005) and stroke work efficiency 18% +/- 10% (p = 0.009) in diabetic animals but not controls. Therefore, oxygen utilization efficiency (stroke work-LVVO(2)) increased only in diabetic animals (16.6% +/- 4.8% to 26.9% +/- 3.6%, p = 0.002) following GIK. CONCLUSIONS: This study provides in vivo evidence that GIK improves LV energetics in diabetes. Oxygen utilization efficiency is improved as a result of improved stroke work efficiency and decreased unloaded LVVO(2). Improved efficiency of oxygen utilization provides a physiologic rationale for the beneficial effect of GIK in diabetic patients.

Direct compression of the failing heart reestablishes maximal mechanical efficiency.

BACKGROUND: In failing hearts, homeostatic mechanisms contrive to maximize stroke work and maintain normal arterial blood pressure at the expense of energetic efficiency. In contrast dobutamine reestablishes maximal mechanical efficiency by promoting energetically optimal loading conditions. However, dobutamine also wastefully increases nonmechanical oxygen consumption. We investigated whether direct mechanical cardiac compression would reestablish maximal mechanical efficiency without the oxygen-wasting effect. METHODS: The pressure-volume relationship and myocardial oxygen consumption were derived in sheep using left ventricular pressure and volume from manometer-tipped and conductance catheters, and coronary flow from Transonics flow probe. RESULTS: Propranolol hydrochloride and atropine sulfate were administered to reduce ejection fraction to 21% when ventricular elastance fell to 1.35 mm Hg/mL and mechanical efficiency to 79% of maximal. Low-pressure direct mechanical compression of the failing heart restored mechanical efficiency to 94% of maximal and realigned optimal left ventricular end-systolic pressure with operating left ventricular end-systolic pressure without altering nonmechanical oxygen consumption. CONCLUSIONS: We conclude that direct cardiac compression restores mechanical efficiency to normal maximum without wasting energy on additional nonmechanical activity.

Cardiomyoplasty reduces myocardial oxygen consumption: implications for direct mechanical compression.

BACKGROUND: This study investigates the possibility of reducing myocardial oxygen consumption by dynamic cardiomyoplasty in chronic heart failure. The sheep model used is relevant for cardiac assist using direct mechanical cardiac compression. METHODS: In 7 sheep, heart failure was induced by staged intracoronary microembolization followed by dynamic cardiomyoplasty. Six months later, the effect of latissimus dorsi muscle stimulation in the 2:1 mode (on, cardiomyoplasty; off, control) was studied. Left ventricular pressure-volume loops were obtained by conductance, micromanometer, and inferior vena cava occlusion catheter. Myocardial oxygen consumption was derived from left main coronary artery blood flow and oxygen content of arterial and coronary sinus blood. RESULTS: Cardiomyoplasty had no significant effect on left ventricular hemodynamic variables such as end-systolic pressure. However, cardiomyoplasty increased stroke volume and ejection fraction significantly by 11% +/- 12% and 11% +/- 10%, respectively. Although pressure-volume area and external work did not increase with cardiomyoplasty, myocardial oxygen consumption decreased by 21% +/- 11%. Therefore, cardiomyoplasty increased myocardial efficiency (external work/myocardial oxygen consumption) by 16% +/- 13%. CONCLUSIONS: Despite limited hemodynamic improvement from dynamic cardiac compression by cardiomyoplasty in sheep with chronic heart failure, myocardial oxygen consumption was significantly reduced. These findings provide a rationale for reverse remodeling of the failing heart using direct mechanical compression.

Functional recovery of the native heart after cardiomyoplasty in sheep with heart failure: passive and dynamic effects of volume loading.

BACKGROUND: Dynamic cardiomyoplasty (d-CMP) encourages reverse remodeling and improved contractility and stroke work (SW) efficiency of the failing native heart. This contrasts with passive cardiomyoplasty (p-CMP), which provides "passive girdling." To further evaluate pump recovery we assessed native left ventricular performance (without assist) 6 months after dynamic and passive CMP in sheep with heart failure with acute volume loading. METHODS: Heart failure (left ventricular ejection fraction 26%+/-8%) induced by coronary microembolization was followed by CMP in 11 sheep. After 8 weeks of muscle "training," paced cardiac assist was undertaken in the d-CMP group (n = 6). Five sheep with heart failure served as controls. Six months later the pressure-volume relationship was derived before and after volume loading by colloid solution. Latissimus dorsi muscle pacing was previously ceased in the d-CMP group. RESULTS: Volume loading increased left ventricular end-diastolic volume and pressure in all groups. After volume loading in d-CMP, the SW and pressure-volume area were increased, and SW efficiency remained unchanged. In p-CMP neither variable changed, whereas in control heart failure SW efficiency decreased due to a rise in pressure-volume area with stable SW. CONCLUSIONS: Based on response to volume loading, the failing native heart after 6 months of d-CMP showed functional recovery from "active girdling," whereas p-CMP prevented functional deterioration through passive girdling. The failing control heart progressively deteriorated.

Glucose-insulin-potassium solution improves left ventricular mechanics in diabetes.

BACKGROUND: The mechanism by which glucose-insulin-potassium solutions enhance recovery of left ventricular function after myocardial ischemia in diabetic patients is not well understood. We evaluated the effect of glucose-insulin-potassium on ventriculoarterial coupling and left ventricular mechanics in a chronic ovine model of diabetes. METHODS: Diabetes was induced in 6 sheep with streptozotocin. After 6 months of diabetes, the response of the left ventricular pressure-volume relationship to 60 minutes of intravenous glucose-insulin-potassium solution (1,000 mL of 5% dextrose in water, 100 IU of regular insulin, 90 mmol of KCl at 1.5 mL x kg(-1) x h(-1)) was determined. RESULTS: Glucose-insulin-potassium solution increased end-systolic elastance 68% (p = 0.01) and improved ventriculoarterial coupling (1.7+/-0.3 to 1.0+/-0.1; p < 0.01). Potential energy decreased 35% (p = 0.01), and pressure-volume area decreased 20% (p = 0.01). However, stroke work did not change; therefore stroke work efficiency increased from 50.1%+/-3.5% to 60.2%+/-5.1% (p = 0.01). CONCLUSIONS: Glucose-insulin-potassium solution improves left ventricular contractility and ventriculoarterial coupling in diabetes. Left ventricular mechanics is improved by decreasing total mechanical work without significantly affecting stroke work, resulting in improved stroke work efficiency. Improved efficiency facilitates understanding of the enhanced tolerance to myocardial ischemia afforded by glucose-insulin-potassium solution.