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Oral treatment with fish oils increased atrial n-3 PUFA levels and reduced vulnerability to induction of AF in this dog model. Modulation of cardiac CX by n-3 PUFAs probably contributes to the antiarrhythmic effects of fish oils.

Background— The objective of this study was to identify the impact of diabetes and related comorbidities, namely chronic renal failure, peripheral vascular disease, and low ejection fraction (<35%), on long-term survival of patients undergoing coronary artery bypass graft surgery. Methods and Results— A unicenter study was conducted on 9125 survivors of isolated coronary artery bypass graft surgery between 1992 and 2002. There were 6581 nondiabetic patients and 2544 diabetics, including 1809 patients with noninsulin-dependent diabetes mellitus and 735 patients with insulin-dependent diabetes mellitus. Cardiac-specific survival at 5 and 10 years was lower in insulin-dependent diabetes mellitus compared with both nondiabetic mellitus patients and patients with noninsulin-dependent diabetes mellitus ( P <0.0001). However, freedom from cardiac-related death was similar for patients with noninsulin-dependent diabetes mellitus and nondiabetes mellitus patients up to 6 years ( P =0 0.08) after surgery and was significantly lower thereafter ( P =0.004). Cardiac-specific survival after coronary artery bypass graft surgery in patients with one or more comorbidities was comparable ( P =0.4) for both nondiabetes mellitus patients and patients with noninsulin-dependent diabetes mellitus, but was significantly lower for those requiring insulin therapy ( P <0.0001). Noninsulin-dependent diabetes mellitus was not an independent predictor of long-term cardiac death (hazard ratio: 1.09, P =0.41); however, insulin-dependent diabetes mellitus, chronic renal failure, peripheral vascular disease, and low ejection fraction were all independent risk factors for late cardiac death (all P <0.0001). The impact of comorbidities on the long-term risk of cardiac death was similar for the 3 groups. Conclusions— Noninsulin-dependent diabetes is not an independent predictor of late cardiac death after coronary artery bypass graft surgery, because cardiac-related survival is similar to that of nondiabetic patients for 6 years after surgery. In diabetic and nondiabetic patients, cardiac survival is adversely affected by the need for insulin therapy and/or the presence and number of comorbidities such as chronic renal failure, peripheral vascular disease, and low ejection fraction.

The intrinsic cardiac nervous system receives reduced input from extracardiac sympathetic efferent neurons after transplantation and inconsistent input from parasympathetic efferent preganglionic neurons. These heterogeneous neuronal inputs are not reflected in heart rate variability or ventricular beta-adrenergic receptor function. Transplanted angiotensin II-sensitive intrinsic cardiac neurons exert greater cardiac control than do nicotine-sensitive ones. The intrinsic cardiac nervous system remodels itself after cardiac transplantation, and this indicates that direct assessment of extracardiac and intrinsic cardiac neuronal behavior is required to fully understand cardiac control after transplantation.

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Diminished infarct size with MK-0852 treatment suggests an additional mechanism of benefit for GPIIb/IIIa blockers beyond stabilization of a "culprit" acute coronary lesion. This cytoprotective effect was unrelated to preservation of coronary vasoreactivity (assessed by reactive hyperemia), restoration of blood flow across the myocardium or acute improvement in contractility.

Impaired renal function is associated with an increased risk for cardiovascular events and death, but the pathophysiology is poorly defined. The hypothesis that coronary blood flow regulation and distribution of ventricular blood flow could be compromised during acute renal failure (ARF) was tested. In two separate groups (n ‫؍‬ 14 each) of dogs with ARF, (1) coronary autoregulation (pressure-flow relations), vascular reserve (reactive hyperemia), and myocardial blood flow distribution (microspheres) and (2) coronary vessel responses to intracoronary infusion of select endothelium-dependent and -independent vasodilators were evaluated. In addition, coronary pressure-flow relations and vascular reserve after inhibition of nitric oxide and prostaglandin release were evaluated. Under resting conditions, myocardial oxygen consumption increased in dogs with ARF compared with no renal failure (NRF; 11.8 ؎ 9.2 versus 5.0 ؎ 1.5 ml O 2 /min per 100 g; P ‫؍‬ 0.01), and the autoregulatory break point of the coronary pressure-flow relation was shifted to higher diastolic coronary pressures (60 ؎ 17 versus 52 ؎ 8 mmHg in NRF; P ‫؍‬ 0.003); the latter was shifted further rightward after inhibition of both nitric oxide and prostaglandin release. The endocardial/epicardial blood flow ratio was comparable for both groups, suggesting preserved ventricular distribution of blood flow. In dogs with ARF, coronary vascular conductance also was reduced (P ‫؍‬ 0.001 versus NRF), but coronary zero-flow pressure was unchanged. Vessel reactivity to each endothelium-dependent/independent compound also was blunted significantly. In conclusion, under resting conditions, coronary vascular tone, reserve, and vessel reactivity are markedly diminished with ARF, suggesting impaired vascular function. Consequently, during ARF, small increases in myocardial oxygen demand would induce subendocardial ischemia as a result of a limited capacity to increase oxygen supply and thereby contribute to higher risk for adverse coronary events and mortality. Several major clinical trials have documented that reduced renal function is associated with increased risk for cardiovascular events and death (2,3) in patients with acute or chronic renal disease (4). Renal disease also is an important risk factor for cardiovascular complications after myocardial infarction and cardiogenic shock (5). Renal failure modifies most factors that regulate cardiovascular function via direct hemodynamic effects, neurogenic reflexes, and circulating hormones (6). The loss of cardiovascular reserve as a result of renal disease may explain the high morbidity and mortality in patients with end-stage renal failure (4,7,8). Coronary autoregulation is an important homeostatic mechanism for maintenance of nutrient and oxygen delivery to the myocardium (9 -11). Intrinsic autoregulatory mechanisms adjust tone within the microvasculature to maintain distribution of myocardial blood flow over a range of oxygen supply and demand requirements (9). Factors that are involved include intra-and ext...