SLEEP APNEA IS A COMMON AND DANGEROUS CARDIOVASCULAR RISK FACTOR.

Sleep apnea involves almost one billion individuals throughout the world, including 40 million Americans. Of major medical concern is the fact that the prevalence of sleep apnea is significantly increasing due to the epidemic of obesity, physical inactivity, and diabetes mellitus which are important risk factors for the development and persistence of sleep apnea in individuals. Sleep apnea is characterized by multiple episodes of apnea or hypopnea during sleep, which cause nocturnal arousals, gasping for breath during the night, daytime sleepiness, irritability, forgetfulness, fatigue and recurrent headaches. Obstructive sleep apnea occurs when upper airway obstruction occurs in an individual during sleep with absent or markedly reduced airflow in the presence of continued activity of inspiratory thoracic and diaphragmatic muscles. Central sleep apnea is defined as the absence or the significant reduction of naso-oral airflow due to the withdrawal during sleep of ponto-medullary respiratory center stimulation of the nerves of the inspiratory thoracic and diaphragmatic muscles and absence of contraction of these muscles during apnea. Complex sleep apnea occurs when an individual exhibits characteristics of both obstructive and central sleep apnea. The severity of sleep apnea is measured by polysomnography and the apnea hypopnea index (AHI), which is the average number of apneas and hypopneas per hour of sleep measured by polysomnography. Sleep apnea is mild if the AHI is 5-14/hour with no or mild symptoms, moderate if the AHI is 15 to 30/hour with occasional daytime sleepiness, and severe if the AHI is >30/hour with frequent daytime sleepiness that interferes with the normal activities of daily life. Chronic sleep apneas and hypopneas followed by compensatory hyperpneas are associated with significant adverse cardiovascular consequences including: 1) recurrent hypoxemia and hypercarbia; 2) Increased sympathetic nerve activity and decreased parasympathetic nerve activity; 3) oxidative stress and vascular endothelial dysfunction; and 4) cardiac remodeling and cardiovascular disease. Moderate or severe sleep apnea significantly increases the risk of coronary artery disease, congestive heart failure, cerebral vascular events (strokes), and cardiac dysrhythmias, and also increase the morbidity and mortality of these diseases. Nevertheless, sleep apnea is currently underdiagnosed and untreated in many individuals due to the challenges in the prediction and detection of sleep apnea and a lack of well-defined optimal treatment guidelines. Chronic continuous positive airway pressure for ≥4 hours/night for >70% of nights is beneficial in the treatment of patients with sleep apnea. CPAP Improves sleep quality, reduces the AHI, augments cardiac output and increases oxygen delivery to brain and heart, reduces resistant hypertension, decreases cardiac dysrhythmias, and reduces daytime sleepiness. The present article discusses the diagnosis of obstructive sleep apnea, central sleep apnea, and complex apnea. Thereafter the important pathophysiologic mechanisms in sleep apnea and the relationship of these pathophysiologic mechanics to atherosclerotic vascular disease are reviewed. Guidelines are then provided for the treatment of mild, moderate and severe sleep apnea In order to reduce the cardiovascular morbidity and mortality caused by sleep apnea and facilitate the diagnosis and the long-term, effective treatment of sleep apnea in patients, the close cooperation is necessary of cardiovascular specialists, pulmonary specialists, and respiratory therapy/ rehabilitation specialists.

The differentiation of the competitive athlete with physiologic cardiac remodeling from the athlete with cardiomyopathy.

There are currently 5 million active high school, collegiate, professional, and master athletes in the United States. Regular intense exercise by these athletes can promote structural, electrical and functional remodeling of the heart, which is termed the "athlete's heart." In addition, regular intense exercise can lead to pathological adaptions that promote or worsen cardiac disease. Many of the athletes in the United States seek medical care. Consequently, physicians must be aware of the normal cardiac anatomy and physiology of the athlete, the differentiation of the normal athlete heart from the athlete with cardiomyopathy, and the contemporary care of the athlete with a cardiomyopathy. In athletes with persistent cardiovascular symptoms, investigations should include a detailed history and physical examination, an ECG, a transthoracic echocardiogram, and in athletes in whom the diagnosis is uncertain, a maximal exercise stress test or a continuous ECG recording, and cardiac magnetic resonance imaging or cardiac computed tomography angiography when definition of the coronary anatomy or characterization of the aorta and the aortic great vessels is indicated. This article discusses the differentiation of the normal athlete with physiologic cardiac remodeling from the athlete with hypertrophic, dilated or arrhythmogenic ventricular cardiomyopathy (ACM). The ECG changes in trained athletes that are considered normal, borderline, or abnormal are listed. In addition, the normal echocardiographic measurements for athletes who consistently participate in endurance, power, combined or heterogeneous sports are enumerated and discussed. Algorithms are listed that are useful in the diagnosis of trained athletes with borderline or abnormal echocardiographic measurements suggestive of cardiomyopathies along with the major and minor criteria for the diagnosis of ACM in athletes. Thereafter, the treatment of athletes with hypertrophic, dilated, and arrhythmogenic right ventricular cardiomyopathies are reviewed. The distinction between physiologic changes and pathologic changes in the hearts of athletes has important therapeutic and prognostic implications. Failure by the physician to correctly diagnose an athlete with hypertrophic cardiomyopathy, dilated cardiomyopathy, or ACM, can lead to the sudden cardiac arrest and death of the athlete during training or sports competition. Conversely, an incorrect diagnosis by a physician of cardiac pathology in a normal athlete can lead to an unnecessary restriction of athlete training and competition with resultant significant emotional, psychological, financial, and long-term health consequences in the athlete.

The diagnosis and treatment of women with recurrent cardiac ischemia and normal coronary arteries.

Cardiac disease is the leading cause of death in women. Among women with recurrent chest pain, abnormal electrocardiograms, and/or stress tests who undergo coronary angiography, as many as 50% have normal or <50% coronary artery obstructive disease. Pharmacologic stress assessment of coronary artery flow reserve in these women frequently demonstrates an inability to increase blood flow to >2.5 times normal flow. Contributory factors include abnormal epicardial or microvascular reactivity, microvascular remodeling or rarefaction, autonomic dysfunction, or coronary plaque rupture/erosion. Assessment is necessary of serum biomarkers and coronary artery flow reserve, fractional flow reserve, microvascular resistance, and epicardial/microvascular spasm. Aggressive treatment of women with positive tests is necessary because these women have an increased incidence of recurrent chest pain, repeated hospitalizations and coronary angiograms, and cardiac death.

Particulate Matter Air Pollution is a Significant Risk Factor for Cardiovascular Disease.

Air pollution is responsible worldwide for 9-12 million deaths annually. The major contributor to air pollution is particulate matter ≤2.5 µg per cubic meter of air (PM2.5) from vehicles, industrial emissions, and wildfire smoke. United States ambient air standards recommend annual average PM2.5 concentrations of ≤12 µg/m³ while European standards allow an average annual PM2.5 concentration of ≤20 µg/m3. However, significant PM2.5 cardiovascular and pulmonary health risks exist below these concentrations. Chronic PM2.5 exposure significantly increases major cardiovascular and pulmonary event risks in Americans by 8 to more than 20% for each 10-µg/m3 increase in PM2.5. PM2.5-induced increases in lipid peroxidation, induction of vascular inflammation and endothelial cell injury initiate and propagate respiratory diseases, coronary and carotid atherosclerosis. PM2.5 can cause atherosclerotic vascular plaque rupture and myocardial infarction and stroke by activating metalloproteinases. This article discusses PM2.5 effects on the cardiovascular and pulmonary systems, specific PM2.5 pathophysiologic mechanisms contributing to cardiopulmonary disease, and preventive measures to limit the cardiovascular and pulmonary effects of PM2.5.

The epidemiology, mechanisms, diagnosis and treatment of cardiovascular disease in adult patients with HIV.

More than 1.2 million people in the United States have Human Immunodeficiency Virus (HIV) infections but 13% of these people are unaware of their HIV infection. Current combination antiretroviral therapy (ART) does not cure HIV infection but rather suppresses the infection with the virus persisting indefinitely in latent reservoirs in the body. As a consequence of ART, HIV infection has changed from a fatal disease in the past to a chronic disease today. Currently in the United States, more than 45% of HIV+ individuals are greater than 50 years of age and 25% will be greater than 65 years of age by 2030. Atherosclerotic cardiovascular disease (CVD), including myocardial infarction, stroke, and cardiomyopathy, is now the major cause of death in HIV+ individuals. Novel risk factors, including chronic immune activation and inflammation in the body, antiretroviral therapy, and traditional CVD risk factors, such as tobacco and illicit drug use, hyperlipidemia, the metabolic syndrome, diabetes mellitus, hypertension, and chronic renal disease, contribute to cardiovascular atherosclerosis. This article discusses the complex interactions involving HIV infection, the novel and traditional risk factors for CVD, and the antiretroviral HIV therapies which can contribute to CVD in HIV-infected people. In addition, the treatment of HIV+ patients with acute myocardial infarction, stroke, and cardiomyopathy/heart failure are discussed. Current recommended ART and their major side effects are summarized in table format. All medical personnel must be aware of the increasing incidence of CVD on the morbidity and mortality in HIV infected patients and must be watchful for the presence of CVD in their patients with HIV.

Cardiovascular complications of COVID-19 severe acute respiratory syndrome.

603,711,760 confirmed cases of COVID-19 have been reported throughout the world and 6,484,136 individuals have died from complications of COVID-19 as of September 7, 2022. Significantly, the Omicron variant has produced the largest number of COVID-19 associated hospitalizations since the beginning of the pandemic. Cardiac injury occurs in ≥20% of the hospitalized patients with COVID-19 and is associated with cardiac dysrhythmias in 17 to 44%, cardiac injury with increases in blood troponin in 22 to 40%, myocarditis in 2 to 7%, heart failure in 4 to 21%, and thromboembolic events in 15 to 39%. Risk factors for cardiac complications include age >70 years, male sex, BMI ≥30 kg/m2, diabetes, pre-existing cardiovascular disease, and moderate to severe pneumonia at hospital presentation. Patients with prior cardiovascular disease who contract COVID-19 and experience a significant increase in their blood troponin concentration are at risk for mortality rates as high as 69%. This review focuses on the prevalence, the pathophysiologic mechanisms of CoV-2 injury to the cardiovascular system and the current recommended treatments in hospitalized patients with COVID-19 in order that medical personnel can decrease the morbidity and mortality of patients with COVID-19 and effectively treat patients with Covid and post Covid syndrome.

Handheld ultrasound as an adjunct to physical examination in the diagnosis of cardiopulmonary disease.

Handheld 2D ultrasound devices (HUDs) have become available as an adjunct to physical examinations, visualizing the heart and lungs in real time and facilitating prompt patient diagnosis and treatment of cardiopulmonar.y disorders. These devices provide simple and rapid bedside alternatives to repetitive chest x-rays, standard ultrasound examinations and thoracic CT scans. Two currently available HUDs are described. This paper discusses the use of HUDs in the diagnosis of patients with pericardial effusion and tamponade, ventricular dilation, aortic and mitral regurgitation, cardiogenic pulmonary edema, viral and bacterial pneumonia, pleural effusion and pneumothorax. The use of a HUD by physicians increases clinical diagnostic accuracy, adds quantitative information about cardiopulmonary disease severity and guides the use of medications and interventions.

Tricuspid valve regurgitation: current diagnosis and treatment.

Tricuspid regurgitation (TR) is present in 1.6 million individuals in the United States and 3.0 million people in Europe. Functional TR, the most common form of TR, is caused by cardiomyopathies, LV valve disease, or pulmonary disease. The five-year survival with severe TR and HFrEF is 34%. Echocardiography can assess the TR etiology/severity, measure RA and RV size and function, estimate pulmonary pressure, and characterize LV disease. Management includes diuretics, ACE inhibitors, and aldosterone antagonists. Surgical annuloplasty or valve replacement should be considered in patients with progressive RV dilatation without severe LV dysfunction and pulmonary hypertension. Transcatheter repair/replacement is possible in patients with a LVEF <40%, dilated annuli, and impaired RV function. The diagnosis and treatment of TR, including coaptation, annuloplasty devices and prosthetic valves, success rates, morbidity/mortality, and trials are discussed. Transcatheter tricuspid valve repair/replacement is an emerging therapy for high-risk patients with TR who would otherwise have a dismal clinical prognosis.

The current diagnosis and treatment of high-risk patients with chronic primary and secondary mitral valve regurgitation.

Mitral valve regurgitation (MR) is due primarily to either primary degeneration of the mitral valve with Barlow's or fibroelastic disease or is secondary to ischemic or nonischemic cardiomyopathies. Echocardiography is essential to assess MR etiology and severity, the remodeling of cardiac chambers and to characterize longitudinal chamber changes to determine optimal therapies. Surgery is recommended for severe primary MR if persistent symptoms are present or if left ventricle dysfunction is present with an EF <60% or a left ventricle end-systolic diameter ≥40 mm. For secondary MR, therapy of heart failure with vasodilators and diuretics improves forward cardiac output. Coronary artery bypass grafts (CABG) or percutaneous coronary intervention (PCI) should be considered for severe MR due to ischemia. This review summarizes the pathophysiology, the characteristics, the management and the different interventions for high risk patients with chronic primary and secondary MR.

Obesity and obesity-induced inflammatory disease contribute to atherosclerosis: a review of the pathophysiology and treatment of obesity.

Two billion people worldwide older than 18 years of age, or approximately 30% of the world population, are overweight or obese. In addition, more than 43 million children under the age of 5 are overweight or obese. Among the population in the United States aged 20 and greater, 32.8 percent are overweight and 39.8 percent are obese. Blacks in the United States have the highest age-adjusted prevalence of obesity (49.6%), followed by Hispanics (44.8%), whites (42.2%) and Asians (17.4%). The impact of being overweight or obese on the US economy exceeds $1.7 trillion dollars, which is equivalent to approximately eight percent of the nation's gross domestic product. Obesity causes chronic inflammation that contributes to atherosclerosis and causes >3.4 million deaths/year. The pathophysiologic mechanisms in obesity that contribute to inflammation and atherosclerosis include activation of adipokines/cytokines and increases in aldosterone in the circulation. The adipokines leptin, resistin, IL-6, and monocyte chemoattractant protein activate and chemoattract monocytes/macrophages into adipose tissue that promote visceral adipose and systemic tissue inflammation, oxidative stress, abnormal lipid metabolism, insulin resistance, endothelial dysfunction, and hypercoagulability that contribute to atherosclerosis. In addition in obesity, the adipokines/cytokines IL-1ß, IL-18, and TNF are activated and cause endothelial cell dysfunction and hyperpermeability of vascular endothelial junctions. Increased aldosterone in the circulation not only expands the blood volume but also promotes platelet aggregation, vascular endothelial dysfunction, thrombosis, and fibrosis. In order to reduce obesity and obesity-induced inflammation, therapies including diet, medications, and bariatric surgery are discussed that should be considered in patients with BMIs>35-40 kg/m2 if diet and lifestyle interventions fail to achieve weight loss. In addition, antihypertensive therapy, plasma lipid reduction and glucose lowering therapy should be prescribed in obese patients with hypertension, a 10-year CVD risk >7.5%, or prediabetes or diabetes.

The current diagnosis and treatment of patients with aortic valve stenosis.

Aortic valve stenosis (AS) is the third most frequent cardiovascular abnormality after coronary artery disease and hypertension. A bicuspid aortic valve is the most common cause for AS until seventh decade and calcific valve degeneration is responsible thereafter. In symptomatic patients, The risk of death increases from ≤1%/year to 2%/month. An echo valve area ≤1 cm2, peak transaortic velocity ≥4 m/s, mean valve gradient ≥40 mmHg and/or computerized tomography valve calcium score >2000 Agatston units (AU) for males or more than 1200 AU for females indicate severe AS. AS stages and management are discussed. Valve replacement is based on surgical risk, valve durability/hemodynamics, need for anticoagulation and patient preferences. EuroSCORE ≥20%, Society of Thoracic Surgeons Predicted Risk of Mortality ≥8% and co-morbidities indicate high surgical risk. Surgery is recommended for low-intermediate risk patients. Transcatheter aortic valve implantation is an alternative in older patients at low, intermediate, high or prohibitive risk. Transaortic valve implantation/replacement trials are summarized.

Cardiovascular Exosomes and MicroRNAs in Cardiovascular Physiology and Pathophysiology.

Cardiac exosomes mediate cell-to-cell communication, stimulate or inhibit the activities of target cells, and affect myocardial hypertrophy, injury and infarction, ventricular remodeling, angiogenesis, and atherosclerosis. The exosomes that are released in the heart from cardiomyocytes, vascular cells, fibroblasts, and resident stem cells are hypoimmunogenic, are physiologically more stable than cardiac cells, can circulate in the body, and are able to cross the blood-brain barrier. Exosomes utilize three mechanisms for cellular communication: (1) internalization by cells, (2) direct fusion to the cell membrane, and (3) receptor-ligand interactions. Cardiac exosomes transmit proteins, mRNA, and microRNAs to other cells during both physiological and pathological process. Cardiac-specific exosome miRNAs can regulate the expression of sarcomeric genes, ion channel genes, autophagy, anti-apoptotic and anti-fibrotic activity, and angiogenesis. This review discusses the role of exosomes and microRNAs in normal myocardium, myocardial injury and infarction, atherosclerosis, and the importance of circulating microRNAs as biomarkers of cardiac disease. Graphical Abstract.

Diagnosis and treatment of adults with congenital heart disease.

Approximately 50 million adults worldwide have known congenital heart disease (CHD). Among the most common types of CHD defects in adults are atrial septal defects and ventricular septal defects followed by complex congenital heart lesions such as tetralogy of Fallot. Adults with CHDs are more likely to have hypertension, cerebral vascular disease, diabetes and chronic kidney disease than age-matched controls without CHD. Moreover, by the age of 50, adults with CHD are at a greater than 10% risk of experiencing cardiac dysrhythmias and approximately 4% experience sudden death. Consequently, adults with CHD require healthcare that is two- to four-times greater than adults without CHD. This paper discusses the diagnosis and treatment of adults with atrial septal defects, ventricular septal defects and tetralogy of Fallot.

Diagnosis and treatment of heart failure with preserved left ventricular ejection fraction.

Nearly six million people in United States have heart failure. Fifty percent of these people have normal left ventricular (LV) systolic heart function but abnormal diastolic function due to increased LV myocardial stiffness. Most commonly, these patients are elderly women with hypertension, ischemic heart disease, atrial fibrillation, obesity, diabetes mellitus, renal disease, or obstructive lung disease. The annual mortality rate of these patients is 8%-12% per year. The diagnosis is based on the history, physical examination, laboratory data, echocardiography, and, when necessary, by cardiac catheterization. Patients with obesity, hypertension, atrial fibrillation, and volume overload require weight reduction, an exercise program, aggressive control of blood pressure and heart rate, and diuretics. Miniature devices inserted into patients for pulmonary artery pressure monitoring provide early warning of increased pulmonary pressure and congestion. If significant coronary heart disease is present, coronary revascularization should be considered.

Recognition and treatment of ischemic heart diseases in women.

Heart disease is the leading cause of death among women in the industrialized world. However, women after myocardial infarctions (MIs) are less likely to receive preventive medications or revascularization and as many as 47% experience heart failure, stroke or die within 5 years. Premenopausal women with MIs frequently have coronary plaque erosions or dissections. Women under 50 years with angina and nonobstructive epicardial coronary artery disease often have coronary microvascular dysfunction (CMD) with reductions in coronary flow reserve that may require nontraditional therapies. In women with coronary artery disease treated with stents, the 3-year incidence of recurrent MI or death is 9.2%. Coronary bypass surgery operative mortality averages 4.6% for women compared with 2.4% in men. Addition of internal mammary artery and radial artery coronary grafts in women does not increase operative survival but improves 5-year outcome to greater than 80%.

Type-2 diabetes mellitus and cardiovascular disease.

The global prevalence of diabetes has risen in adults from 4.7% in 1980 to 8.5% in 2014. 90-95% of adults with diabetes have Type 2 diabetes (T2D). This paper focuses on the diagnosis and treatment of T2D patients who have or are at risk for cardiovascular disease. Hyperglycemia, insulin resistance and excess fatty acids increase oxidative stress, disrupt protein kinase C signaling and increase advanced glycation end-products that result in vascular inflammation, vasoconstriction, thrombosis and atherogenesis. Intensive T2D treatment produces a ≥10% risk reduction in major macrovascular and microvascular events. Glucose-lowering therapies must be individualized. Metformin is an optimal drug for monotherapy. If hemoglobin A1c is not at goal, a sodium-glucose cotransporter-2 inhibitor or a dipeptidyl peptidase-4 inhibitor should be considered for therapy with metformin. Coronary angioplasty/stenting is recommended for diabetic patients with acute myocardial infarctions. Coronary artery bypass grafting is recommended for symptomatic diabetic patients with multivessel disease.

Poly(ADP-ribose) Polymerase (PARP) and PARP Inhibitors: Mechanisms of Action and Role in Cardiovascular Disorders.

Poly(ADP-ribosyl)ation is an immediate cellular repair response to DNA damage and is catalyzed primarily by poly(ADP-ribose)polymerase-1 (PARP1), which is the most abundant of the 18 different PARP isoforms and accounts for more than 90% of the catalytic activity of PARP in the cell nucleus. Upon detection of a DNA strand break, PARP1 binds to the DNA, cleaves nicotinamide adenine dinucleotide between nicotinamide and ribose and then modifies the DNA nuclear acceptor proteins by formation of a bond between the protein and the ADP-ribose residue. This generates ribosyl-ribosyl linkages that act as a signal for other DNA-repairing enzymes and DNA base repair. Extensive DNA breakage in cells results in excessive activation of PARP with resultant depletion of the cellular stores of nicotinamide adenine dinucleotide (NAD+) which slows the rate of glycolysis, mitochondrial electron transport, and ultimately ATP formation in these cells. This paper focuses on PARP in DNA repair in atherosclerosis, acute myocardial infarction/reperfusion injury, and congestive heart failure and the role of PARP inhibitors in combating the effects of excessive PARP activation in these diseases. Free oxygen radicals and nitrogen radicals in arteries contribute to disruption of the vascular endothelial glycocalyx, which increase the permeability of the endothelium to inflammatory cells and also low-density lipoproteins and the accumulation of lipid in the vascular intima. Mild inflammation and DNA damage within vascular cells promote PARP1 activation and DNA repair. Moderate DNA damage induces caspase-dependent PARP cleavage and vascular cell apoptosis. Severe DNA damage due to vascular inflammation causes excessive activation of PARP1. This causes endothelial cell depletion of NAD+ and ATP, downregulation of atheroprotective SIRT1, necrotic cell death, and ultimately atherosclerotic plaque disruption. Inhibition of PARP decreases vascular endothelial cell adhesion P-selectin and ICAM-1 molecules, inflammatory cells, pro-death caspase-3, and c-Jun N-terminal kinase (JNK) activation and upregulates prosurvival extracellular signal-regulated kinases and AKT, which decrease vascular cell apoptosis and necrosis and limit atherosclerosis and plaque disruption. In myocardial infarction with coronary occlusion then reperfusion, which occurs with coronary angioplasty or thrombolytic therapy, reperfusion injury occurs in as many as 31% of patients and is caused by inflammatory cells, free oxygen and nitrogen radicals, the rapid transcriptional activation of inflammatory cytokines, and the activation of PARP1. Inhibition of PARP attenuates neutrophil infiltration and inflammatory cytokine expression in the reperfused myocardium and preserves myocardial NAD+ and ATP. In addition, PARP inhibition increases the activation of myocyte survival enzymes protein kinase B (Akt) and protein kinase C epsilon (PKCε), and decreases the activity of myocardial ventricular remodeling enzymes PKCα/ß, PKCζ/λ, and PKCδ. As a consequence, cardiomyocyte and vascular endothelial cell necrosis is decreased and myocardial contractility is preserved. In heart failure and circulatory shock in animal models, PARP inhibition significantly attenuates decreases in left ventricular systolic pressure, ventricular contractility and relaxation, stroke volume, and increases survival by limiting or preventing upregulation of adhesion molecules, proinflammatory cytokines, myocardial mononuclear cell infiltration, and PKCα/ß and PKC λ/ζ. In this manner, PARP inhibition partially restores the myocardial concentrations of NAD+, limits ventricular remodeling and fibrosis, and prevents significant decreases in myocardial contractility. Based primarily on investigations in preclinical models of atherosclerosis, myocardial infarction, and heart failure, PARP inhibition appears to be beneficial in limiting or inhibiting cardiovascular dysfunction. These studies indicate that investigations of acute and chronic PARP inhibition are warranted in patients with atherosclerotic coronary artery disease.

Current status of stem cells in cardiac repair.

One out of every two men and one out of every three women greater than the age of 40 will experience an acute myocardial infarction (AMI) at some time during their lifetime. As more patients survive their AMIs, the incidence of congestive heart failure (CHF) is increasing. 6 million people in the USA have ischemic cardiomyopathies and CHF. The search for new and innovative treatments for patients with AMI and CHF has led to investigations and use of human embryonic stem cells, cardiac stem/progenitor cells, bone marrow-derived mononuclear cells and mesenchymal stem cells for treatment of these heart conditions. This paper reviews current investigations with human embryonic, cardiac, bone marrow and mesenchymal stem cells, and also stem cell paracrine factors and exosomes.

Cardio-oncology: cardiovascular complications of cancer therapy.

This paper focuses on three classes of commonly used anticancer drugs, which can cause cardiotoxicity: anthracyclines, monoclonal antibodies exemplified by trastuzumab and tyrosine kinase inhibitors. Anthracyclines can induce cardiomyocyte necrosis and fibrosis. Trastuzumab can cause cardiac stunning. The tyrosine kinase inhibitors can increase systemic arterial pressure and impair myocyte contractility. In addition, radiation therapy to the mediastinum or left chest can exacerbate the cardiotoxicity of these anticancer drugs and can also cause accelerated atherosclerosis, myocardial infarction, heart failure and arrhythmias. Left ventricular ejection fraction measurements are most commonly used to assess cardiac function in patients who receive chemo- or radiation-therapy. However, echocardiographic determinations of global longitudinal strain are more sensitive for detection of early left ventricular systolic dysfunction. Information on patient-risk stratification and monitoring is presented and guidelines for the medical treatment of cardiac dysfunction due to cancer therapies are summarized.

Acrolein Can Cause Cardiovascular Disease: A Review.

Acrolein is a highly reactive unsaturated aldehyde that is formed during the burning of gasoline and diesel fuels, cigarettes, woods and plastics. In addition, acrolein is generated during the cooking or frying of food with fats or oils. Acrolein is also used in the synthesis of many organic chemicals and as a biocide in agricultural and industrial water supply systems. The total emissions of acrolein in the United States from all sources are estimated to be 62,660 tons/year. Acrolein is classified by the Environmental Protection Agency as a high-priority air and water toxicant. Acrolein can exert toxic effects following inhalation, ingestion, and dermal exposures that are dose dependent. Cardiovascular tissues are particularly sensitive to the toxic effects of acrolein based primarily on in vitro and in vivo studies. Acrolein can generate free oxygen radical stress in the heart, decrease endothelial nitric oxide synthase phosphorylation and nitric oxide formation, form cytoplasmic and nuclear protein adducts with myocyte and vascular endothelial cell proteins and cause vasospasm. In this manner, chronic exposure to acrolein can cause myocyte dysfunction, myocyte necrosis and apoptosis and ultimately lead to cardiomyopathy and cardiac failure. Epidemiological studies of acrolein exposure and toxicity should be developed and treatment strategies devised that prevent or significantly limit acrolein cardiovascular toxicity.