Magnetic resonance imaging findings in apical ballooning syndrome or takotsubo cardiomyopathy.

Cardiac magnetic resonance imaging (CMRI) plays an important role in the diagnosis and follow-up of apical ballooning syndrome (takotsubo syndrome), a recently described cardiac condition characterised by transient dyskinesia of the left ventricle secondary to an acute emotional event. We present the CMRI findings in a 53-year-old female diagnosed with apical ballooning syndrome and discuss its value in the diagnosis and follow-up of this condition.

Predictors of in-stent restenosis and patient outcome after percutaneous coronary intervention in patients with diabetes mellitus.

Diabetics have a significantly higher incidence of major adverse cardiac events (MACEs) and in-stent restenosis (ISR) than nondiabetics after percutaneous coronary intervention (PCI). Predictors of MACEs and ISR are uncertain in diabetics. In recent studies, microalbuminuria and proliferative retinopathy have been believed to relate to progressive coronary atherosclerosis. We retrospectively studied 191 consecutive patients (mean age 65 +/- 9 years) with diabetes who underwent PCI to determine predictors of ISR and MACEs (defined as cumulative incidence of myocardial infarction, revascularization, or death from cardiovascular cause), with special reference to microalbuminuria and proliferative retinopathy. Of 191 patients, 106 (56%) had a follow-up coronary angiogram at 16 +/- 2 months. Of these 106 patients, 66 (62%) developed ISR. In the multivariate model, microalbuminuria or proliferative retinopathy did not achieve significant association with ISR. Serum high-density lipoprotein cholesterol levels were significantly associated with a lower incidence of ISR (odds ratio [OR] 0.928, 95% confidence interval [CI] 0.876 to 0.983, p = 0.011) and MACEs (OR 0.96, 95% CI 0.931 to 1.000, p = 0.048). Use of drug-eluting stents also had a negative association with ISR (OR 0.171, 95% CI 0.05 to 0.585, p = 0.004). Renal insufficiency was associated with higher MACEs (OR 3.19, 95% CI 1.45 to 7.031, p = 0.0039). In conclusion, serum high-density lipoprotein cholesterol levels were inversely associated with ISR or MACEs.

Ectopic fat accumulation and metabolic syndrome.

The recent escalation of obesity from an individual health problem to a major public health issue reaching epidemic proportions has drawn attention to a constellation of abnormalities (abdominal obesity, hypertension and dyslipidaemia) collectively referred to as metabolic syndrome. As an indicator of insulin resistance and a harbinger of diabetes, this syndrome has been associated with major cardiovascular mortality and morbidity. Yet, the exact pathophysiological events leading to the development of metabolic syndrome remain unknown. We review some of the current literature on the pathogenesis of metabolic syndrome with an emphasis on the role of ectopic lipid accumulation.

Single coronary artery with prepulmonic coursing left main coronary artery manifesting as prinzmetal's angina.

We report the case of a 32-year-old man who presented at the emergency department with severe chest pressure, left arm pain, and dizziness. These symptoms were described as intermittent, occurring after exercise and at rest. He had undergone several stress tests during the past 8 years, but no objective evidence of ischemia was produced. His history of hyperlipidemia and increasing frequency of symptoms prompted us to perform coronary angiography, which showed a single coronary artery with an ostium at the right sinus of Valsalva. The vessel had an initial, mixed common trunk that gave rise to both the right coronary artery proper and to the left coronary artery. The left main trunk followed a prepulmonic course. The anatomic features were eventually confirmed by computed tomographic angiography. The left main stem had a fixed 50% to 60% area narrowing, at baseline study. A treadmill stress myocardial perfusion study showed no evidence of ischemia. The patient was referred to a 2nd facility, where intravascular ultrasonography, at baseline, revealed 63% left main narrowing without evidence of atherosclerosis. Acetylcholine provocation demonstrated worsening of the stenosis to about 80%, with reproduction of angina and ST-segment depression, which indicated that medical management of spasm might provide symptomatic relief.

A review of thiazolidinediones and metformin in the treatment of type 2 diabetes with focus on cardiovascular complications.

The rising incidence of obesity and insulin resistance to epidemic proportions has closely paralleled the surge in the prevalence of diabetes and outpaced therapeutic advances in diabetes prevention and treatment. Current evidence points to obesity induced oxidative stress and chronic inflammation as the common denominators in the evolution of insulin resistance and diabetes. Of all the hypoglycemic agents in the pharmacological arsenal against diabetes, thiazolidinediones, in particular pioglitazone, as well as metformin appear to have additional effects in ameliorating oxidative stress and inflammation; rendering them attractive tools for prevention of insulin resistance and diabetes. In addition to their hypoglycemic and lipid modifying properties, pioglitazone and metformin have been shown to exert anti-oxidative and anti-inflammatory effects in vascular beds, potentially slowing the accelerated atherosclerosis in diabetes, which is the major cause of morbidity and mortality in the affected population. The combination of pioglitazone and metformin would thus appear to be an effective pharmacological intervention in prevention and treatment of diabetes. Finally, this review will address the currently available evidence on diabetic cardiomyopathy and the potential role of combination therapy with pioglitazone and metformin.

The prevention and treatment of metabolic syndrome and high-risk obesity.

PURPOSE OF REVIEW: The prevalence of obesity is increasing at an alarming rate, and the obesity epidemic is driving the epidemic in type 2 diabetes. High-risk obesity is characterized by abdominal obesity with evidence of abnormal glucose and lipid metabolism, and a state of heightened inflammation. RECENT FINDINGS: With increasing body weight, lipid accumulation occurs not only in adipose tissue, but in other organs as well. This 'lipotoxicity' in liver, muscle, islets, and elsewhere may account for many of the features of the metabolic syndrome. Adipose tissue produces many proteins, some of which are inflammatory cytokines, and others of which are antiinflammatory or which improve insulin sensitivity. SUMMARY: The treatment of obesity requires the identification of the high-risk patient, and the institution of lifestyle measures with a long-term outlook, and an avoidance of heavily marketed fads. Current research will likely lead to improved medications in the future.

Cardioprotective effects of rosiglitazone are associated with selective overexpression of type 2 angiotensin receptors and inhibition of p42/44 MAPK.

Current evidence points to renin-angiotensin system as a key mediator in ischemia-reperfusion injury. Rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligand, has recently been shown to confer cardioprotection against ischemia-reperfusion in animal models. We sought to examine the expression of ANG II receptors during PPAR-gamma-mediated cardioprotection. Male Sprague-Dawley rats (nondiabetic) were fed either regular rat chow (control diet group, n = 9) or rosiglitazone-rich diet (rosiglitazone-rich diet group, n = 9) and were subjected to 1 h of myocardial ischemia followed by 1 h of reperfusion. A third group of rats had only thoracotomy and pericardiotomy and served as a sham control group (n = 9). Hemodynamics, infarct size, and expression of ANG II type 1 and type 2 receptors (AT1 and AT2) were measured in all groups. There was a 58% reduction of infarct size in the rosiglitazone-rich diet group (P < 0.01 vs. control diet group). Increased myocardial expression of AT(1) receptors in the ischemic-reperfused myocardium was attenuated in the rosiglitazone-rich diet group (P < 0.05 vs. control diet group). Importantly, myocardial AT2 mRNA and protein expression were significantly increased (by >100-fold) in the rosiglitazone-rich diet group (P < 0.05). These changes were accompanied by inhibition of p42/44 MAPK in the rosiglitazone-rich diet group, while the Akt1 expression, believed to mediate insulin sensitization, remained similar in all three groups. The cardioprotective effects of rosiglitazone against myocardial ischemia-reperfusion injury are independent of its insulin-sensitizing properties and are associated with significant overexpression of AT2 receptors along with inhibition of p42/44 MAPK.

Oxidative stress in diabetes: a mechanistic overview of its effects on atherogenesis and myocardial dysfunction.

Diabetes is a major risk factor for atherosclerosis. Atherogenesis involves endothelial dysfunction, activation and injury, inflammation, and smooth muscle cell migration and proliferation. Platelet activation in the narrowed arteries is the most proximate event in the culmination of an acute event such as acute myocardial infraction and stroke. Hyperglycemia is associated with all these adverse events in the process of genesis of atherosclerosis. The effect of diabetes (hyperglycemia) is mediated in large part by the state of enhanced oxidative stress, which is not counter-balanced by endogenous antioxidants. This paper reviews the ignition of oxidative stress in diabetes and the mediation of events leading to atherogenesis.

Trends in the care of patients with acute myocardial infarction at a university-affiliated Veterans Affairs Medical Center.

BACKGROUND: Acute cardiac care of the veterans at Veterans Administration (VA) hospitals has been thought of as poor in quality. We examined the use of life-saving, evidence-based medical therapy in patients admitted with acute myocardial infarction to the University of Arkansas for Medical Sciences-affiliated VA Medical Center in Little Rock and compared the use of this therapy with other hospitals in Arkansas and in the rest of the nation. METHODS: Use of life-saving medical therapy in 117 patients admitted with acute myocardial infarction from January 2002 to December 2002 was compared with the National Registry of Myocardial Infarction database for the identical period. RESULTS: Heparin/low-molecular-weight heparin and glycoprotein IIb/IIIa inhibitors were used in 88% and 66% of patients, respectively. Aspirin, beta adrenergic-blocking agents, angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs), and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) were used in 92%, 93%, 62%, and 79% of the patients, respectively. The use of these therapies was better than in similar patients in Arkansas (P < .001) and the United States as a whole (P < .01). Calcium-channel blockers were used in 16% of the patients. At a mean follow-up period of 1.5 years, use of beta blockers and aspirin had decreased, whereas the use of statins and ACE inhibitors/ARBs was unchanged. CONCLUSION: This study shows that patients with acute myocardial infarction admitted to this university-affiliated VA Medical Center receive evidence-based life-saving medical therapy more often than in the rest Arkansas or in the entire United States. More important, patients at this federal institution continue to receive life-saving medical therapy during follow-up. Better use of evidence-based therapy may be related to affiliation of this VA Medical Center with a teaching institution where board certified cardiologists are involved in short- and long-term care of these patients.

Oxidative stress in cardiovascular disease: molecular basis of its deleterious effects, its detection, and therapeutic considerations.

PURPOSE OF REVIEW: The adoption of immediate reperfusion strategies to treat acutely occluded coronary arteries and the emergence of high-resolution molecular biology techniques have drawn attention to oxidative stress and reactive oxygen species generation in the cardiovascular system. Recent evidence suggests that oxidative stress is a common denominator in many aspects of cardiovascular pathogenesis. This review outlines the current understanding of reactive oxygen species generation and their role in cardiovascular pathophysiology, including atherogenesis, acute myocardial infarction, and congestive heart failure. RECENT FINDINGS: Recent studies highlighting endothelial dysfunction as a response to oxidative stress are of particular interest, as are the findings linking myocardial lipid accumulation (cardiac lipotoxicity) and peroxidation to congestive heart failure. Finally, newer methods to detect reactive oxygen species, including urine assays for measurement of 8,12 iPGF2alpha VI along with nuclear magnetic resonance, can help quantitate the reactive oxygen species burden noninvasively. SUMMARY: The body of current evidence from in vitro studies indicates that oxidative stress plays a major role in cardiovascular disease but the details of molecular events in vivo and in particular in humans remains to be determined. This could partly explain the failure of antioxidant therapy in preventing cardiovascular morbidity and mortality in major clinical trials. The emerging technologies, including MRI, can help delineate the events leading to reactive oxygen species generation and dissipation in humans, and potentially provide a more precisely targeted therapy for the population at risk.

Peroxisome proliferator-activated receptor ligands as antiatherogenic agents: panacea or another Pandora's box?

Peroxisome proliferator activated receptors (PPARs) are members of the nuclear receptor super family that modulate gene expression upon ligand activation. They are 3 major subtypes of PPARs: alpha, delta (also called beta), and gamma. PPAR-gamma is widely expressed in the cardiovascular system and is involved in the regulation of tissue inflammation and smooth muscle cell growth pathways as well as in lipoprotein metabolism and coagulation cascades. PPAR-gamma ligands of (e.g., rosigitazone and pioglitazone) have been shown to exert antiatherogenic effects both in vitro and in vivo. PPAR-alpha ligands (e.g., clofibrate and benzofibrate) modulate lipoprotein metabolism, and affect inflammation and coagulation cascade. These effects may be helpful in resolving the dilemma arising from studies that showed significant mortality and morbidity benefits of fibrates in the face of minimal changes in HDL-cholesterol levels. The role of PPAR-delta in atherogenesis remains largely unknown, although it appears that PPAR-delta activation affects lipoprotein metabolism. PPAR ligands appear to be promising agents in limiting atherosclerosis; however, large-scale clinical trials are required to assess their safety and efficacy before they can be added to the clinicians' arsenal of antiatherosclerotic agents.