Malignancy: An Adverse Effect of Immunosuppression

Benefits of solid organ transplantation in end stage organ diseases are indisputable. Malignancy is a feared complication of solid organ transplantation and is a leading cause of mortality in patients with organ transplantation. Iatrogenic immunosuppression to prevent graft rejection plays a crucial role in the cancer development in solid organ transplant recipients. Chronic exposure to immunosuppression increases the malignancy burden through deregulation of host immune defense mechanisms and unchecked proliferation of oncogenic viruses and malignancies associated with these viruses. Vigorous screening of candidates undergoing transplant evaluation for malignancies, careful assessment of donors, and vigilant monitoring of transplant recipients are necessary to prevent, detect, and manage this life-threatening complication

Managing Cardiovascular Risk in the Post Solid Organ Transplant Recipient

Solid organ transplantation is an effective treatment for patients with end-stage organ disease. The prevalence of cardiovascular diseases (CVD) has increased in recipients. CVD remains a leading cause of mortality among recipients with functioning grafts. The pathophysiology of CVD recipients is a complex interplay between preexisting risk factors, metabolic sequelae of immunosuppressive agents, infection, and rejection. Risk modification must be weighed against the risk of mortality owing to rejection or infection. Aggressive risk stratification and modification before and after transplantation and tailoring immunosuppressive regimens are essential to prevent complications and improve short-term and long-term mortality and graft survival

The dilemma, causes and approaches to avoid recurrent hospital readmissions for patients with chronic heart failure

Heart failure is a progressive illness that carries significant morbidity and mortality. This highly prevalent illness leads to frequent, costly hospitalizations with approximately 50% of patients being readmitted within 6 months of initial hospitalization. While rehospitalization has been extensively studied in the past, little progress has been made in terms of reducing readmission rates of heart failure patients in the last decade despite increasing costs with impending resource limitations. We discuss disease-centered, physician-centered, and patient-centered factors that lead to rehospitalization as well as community/resource availability factors that contribute to rehospitalization of patients suffering from chronic heart failure. In addition, predictors of hospitalization and interventions that reduce hospitalization will be critically evaluated. With a complete understanding of heart failure rehospitalization, we hope the future holds more effective ways to prevent heart failure progression and thus rehospitalization, improved risk-stratification models to identify patients high-risk for rehospitalization, and sustained interventions that are customized according to the etiology of the clinical decline of heart failure patients that ultimately results in frequent rehospitalizations

Persistent Chest Pain and No Obstructive Coronary Artery Disease

Patients with persistent chest pain and no obstructive coronary artery disease are often labeled as having noncardiac pain and not offered further cardiologic testing or treatment. Diagnostic uncertainty for persistent chest pain is associated with adverse quality of life, morbidity, and health care costs. Two underdiagnosed cardiac causes for persistent chest pain include microvascular coronary disease and abnormal cardiac nociception. Microvascular coronary disease is associated with an increased risk of adverse cardiovascular events such as myocardial infarction, congestive heart failure, and sudden cardiac death, and treatment directed at improving endothelial function can improve outcomes. Abnormal cardiac nociception is also a cause for persistent chest pain caused by heightened coronary pain perception. Coronary reactivity testing allows for direct measurement of blood flow characteristics in response to vasoactive agents for the diagnoses of microvascular coronary disease and can be a useful tool to differentiate causes of chest pain. Coronary reactivity testing is an invasive method for assessing coronary vascular function, with current evidence suggesting that its associated risk is relatively low compared with the adverse prognosis associated with microvascular coronary dysfunction. Accurate diagnosis in patients with persistent chest pain and normal coronary arteries can be challenging and deserves adequate investigation in light of the associated morbidity, mortality, and health care costs

Management of Pain

Management of patients with persistent angina and no obstructive coronary artery disease continues to be a challenging area. Currently, pharmacotherapy used in patients with microvascular coronary dysfunction (MCD) is targeted at their underlying mechanism for pain. Therapies used in patients with coronary artery disease such as nitrates, β-blockers, calcium channel blockers, and statins have also been found to be beneficial in those with MCD. Other agents found to have promising effects on anginal symptoms includes ranolazine and angiotensin converting enzyme inhibitors. Hormone therapy in women with MCD improves quality of life, although improvement in myocardial ischemia remains to be determined. In patients with cardiac syndrome X, small trials have been performed showing either beneficial or indeterminate results with the use of other pharmacologic agents such as tricyclic medications, L-arginine, xanthine derivatives, n-3 polyunsaturated fatty acids, nicorandil, and trimetazidine. Non-pharmacologic therapies in the management of chronic angina also play an important role. Lifestyle modification, exercise, and cognitive behavioral therapy have shown to improve angina and exercise capacity in those with MCD. The use of neurostimulation, including transcutaneous electrical nerve stimulation and spinal cord stimulation, can also improve symptoms in those with chronic angina. Incorporating both pharmacologic and non-pharmacological therapies can lead to the effective management of chronic angina in patients with MCD

Erectile Dysfunction as a Complication of Heart Failure

Erectile dysfunction (ED) is an increasingly common problem in the aging population and has been associated with chronic heart failure (HF), either as an epiphenomenon or even as an early marker for underlying cardiovascular disease. ED has a significant effect on patients’ quality of life. This chapter reviews ED in patients with HF and prevention and treatment based on current data from the literature. Causes include physiologic changes resulting in decreased cardiac function and exercise capacity, intrinsic vascular and neurohormonal abnormalities, and extrinsic factors such as medication side effects and psychological issues. Physicians should address these issues with patients and begin treatment by optimizing HF management and minimizing medications with ED side effects. Use of phosphodiesterase-5 inhibitors provides significant improvement of ED and quality of life. Further research still is needed regarding long-term effects of ED treatment, investigation of newer medications, and preventive measures in this patient population

Is Vitamin D Deficiency Associated With Heart Failure? A Review of Current Evidence

An estimated 1 billion people worldwide have deficient or insufficient levels of vitamin D. Even more alarming is the association of vitamin D deficiency with many types of diseases, particularly heart failure (HF). Hypovitaminosis D has been observed to be highly prevalent in the HF community with rates varying from approximately 80% to 95%. Higher rates of deficiency have been linked to winter months, in patients with protracted decompensated HF, darker skin pigmentation, and higher New York Heart Association (NYHA) classes. In fact, some data suggest vitamin D deficiency may even be an independent predictor of mortality in patients with HF. Traditionally obtained through UV exposure and activated in the liver and then the kidneys, vitamin D is classified as a vitamin but functions as a steroid hormone. The hormone acts through the vitamin D receptor (VDR), which is expressed in vascular smooth muscle cells, renal juxtaglomerular cells, and most interestingly, cardiac myocytes. Studies have shown that the association between vitamin D deficiency and HF often manifests in the structural components of cardiac myocytes and/or through alterations of the neurohormonal cascade. In addition, vitamin D may also act rapidly through intracellular nongenomic receptors that alter cardiac contractility. Unfortunately, prospective vitamin D supplementation trials show mixed results. In rat models, successful correction of deficiency was associated with reductions in ventricular hypertrophy. In humans, however, echocardiographic dimensions did not change significantly. These results bring into questions whether vitamin D is a risk factor for HF, a marker of HF disease severity, or has a true pathologic role. This article provides a thorough review of vitamin D deficiency etiology, prevalence, and possible pathophysiologic role in HF. Furthermore, we carefully review prospective trials on vitamin D therapy in HF. We believe more trials on vitamin D therapy in HF need to be conducted before any conclusions can be drawn