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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary arteries in diabetic patients appear to be narrower than in normal subjects, but this has not been examined systematically. To investigate this hypothesis we reviewed the data of 711 consecutive patients with angiographically 'normal coronary arteries'. Excluded were patients with valvular, myocardial or pericardial disease, and patients with hypertension or hyperlipidemia. Thirteen diabetic patients (10 men) and 22 nondiabetic persons (8 men) constituted the study and control groups, respectively. The diameters of the coronary arteries and their branches were measured and adjusted for body surface area. The sum of the proximal left anterior descending (LAD), circumflex and right coronary arteries (RCA) was calculated and defined as total coronary diameter (TCD). The sum of the distal LAD, first diagonal, first marginal and distal RCA was calculated and defined as total distal coronary diameter (dTCD). The clinical data of both groups were comparable. Adjusted TCD for body surface area was 5.4 +/- 1.1 and 6.5 +/- 1.1 mm/m2 (p < 0.05) in diabetics and nondiabetics, respectively, and adjusted dTCD was 4.9 +/- 1.2 and 6.1 +/- 1.2 mm/m2 (p = 0.01) in diabetics and normal subjects, respectively. Specific arteries and branches that were significantly smaller in diabetics included: left main coronary artery, distal LAD, first diagonal, proximal RCA, distal RCA, right ventricular branch, and posterolateral and posterior descending artery of RCA origin. Gender was not a confounding factor since the control group had a larger proportion of women and still larger arteries than the diabetic group. In conclusion, coronary arteries and their branches in diabetic patients have smaller diameters than normal subjects. This may be due to increased coronary tone, diffuse mild atherosclerosis or both.
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PMID:Diffuse narrowing of coronary arteries in diabetic patients: the earliest phase of coronary artery disease. 952 10

Cardiac disease constitutes a common complication among patients with renal failure. This is partly due to the high incidence of shared risk factors, such as hypertension or diabetes mellitus, and some to specific factors inherent in renal disease. It implies a high incidence of cardiac failure and ischemic heart disease (frequently without significant coronary artery obstructions) with important associated morbidity and mortality. Pericardial disease, valvular involvement and arrhythmia are also common among these patients. The management of these complications in patients with endstage renal disease has some particularities, specially in the field of drug therapy.
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PMID:[Cardiac pathology of extracardiac origin (IX)> Cardiac pathology in the patient with chronic nephropathy]. 966

Cardiac tamponade is an extremely rare manifestation of systemic sclerosis and has been reported to be a risk factor for the subsequent development of renal failure. We report the case of a 37-year-old man with recently diagnosed scleroderma who presented with chest pain and shortness of breath. He was found to have scleroderma renal crisis as well as cardiac tamponade. He responded hemodynamically to emergent pericardiocentesis and blood pressure control with angiotensin-converting enzyme inhibitors. However, the renal function deteriorated further leading to development of end-stage renal disease and required chronic hemodialysis.Although pericardial effusions are common in scleroderma, cardiac tamponade is rare. Coexistent hypertension and cardiac tamponade in scleroderma have not been described previously. Elevated systemic blood pressure can accompany and should not be used to exclude the diagnosis of cardiac tamponade. We emphasize the importance of pericardial disease as an uncommon but important cause of chest pain in patients with scleroderma.
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PMID:Cardiac tamponade: an uncommon presentation of hypertensive scleroderma renal crisis. 1704 85

Heart failure has emerged as a dominant form of cardiovascular disease in Africa, and has great social and economic relevance owing to its high prevalence, mortality and impact on young, economically active individuals. The causes of heart failure in Africans remain largely nonischemic. Hypertension, cardiomyopathy, rheumatic heart disease, chronic lung disease and pericardial disease are the main contributors to the etiology of cardiac failure in sub-Saharan Africa, accounting for over 90% of cases. Hypertensive heart disease complications occur more frequently in Africans and the majority of affected patients are younger. Endemic cardiomyopathies include dilated cardiomyopathy, peripartum cardiomyopathy and endomyocardial fibrosis. Nonendemic cardiomyopathies apparently occur with the same frequency as in other parts of the world, and include hypertrophic cardiomyopathy and arrhythmogenic right ventricular dysplasia/cardiomyopathy. Coronary artery disease and its complications remain uncommon in Africa, but the situation is changing due to modifications in lifestyle, risk-prone behavior, diet, cultural attitudes and other consequences of rapid urbanization. As the prevalence of heart failure is expected to rise substantially in sub-Saharan Africa, the authors call for population-based studies and registries of the epidemiology of heart failure in Africans and the urgent study of interventions that will decrease morbidity and mortality from the causes of heart failure, with a focus both on nonischemic and ischemic risk factors.
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PMID:Epidemiology of heart failure in sub-Saharan Africa. 1921 Feb 13

Symptomatic intradialytic hypotension (IH) continues to be an important complication of hemodialysis treatment. It has been suggested that patients with left ventricular (LV) diastolic dysfunction may be more sensitive to the effects of reduced cardiac filling. Left atrial volume index (LAVi) reflects the chronicity of exposure to elevated LV filling pressures. The aim of this study was to identify the association between echocardiographic disease, in particular left atrium enlargement, and IH. Echocardiograms obtained in 172 patients undergoing hemodialysis in sinus rhythm and with no significant valvular or pericardial disease were analyzed. The independent association between LAVi and IH was assessed using multivariate logistic regression. IH was identified in 27 patients (16%). The patients who experienced the hypotensive episodes had a greater prevalence of previous heart failure (59% vs 22%, P < 0.001), systolic dysfunction (33% vs 14%, P = 0.003), and LAVi > 35 mL/m(2) (59% vs 32%, P = 0.008). No differences were noted for age, gender, body mass index, duration of dialysis, blood pressure, use of drugs, and proportions of arterial hypertension, diabetes, LV hypertrophy and diastolic dysfunction by Doppler. After multivariate analysis, only heart failure and LAVi > 35 mL/m(2) were seen to be independent predictors of IH. The finding of left atrium enlargement in patients undergoing hemodialysis may be useful in the clinical prediction of IH.
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PMID:Association between left atrium enlargement and intradialytic hypotension: role of diastolic dysfunction in the hemodynamic complications during hemodialysis. 1948 20

Cardiotoxicity of anticancer treatments has become an increasingly important clinical problem faced by cardiologists. Left ventricular systolic dysfunction and heart failure generate the most concern, but clinical features and prognosis vary considerably depending on the causative agent. Anthracycline-related cardiomyopathy differs fundamentally from effects associated with newer targeted agents, such as trastuzumab. Other forms of cardiovascular disease that occur as a result of cancer treatment include hypertension, thromboembolic disease, pericardial disease, arrhythmia, and myocardial ischemia. The approach to cardiovascular disease in patients with cancer is often different from that in the general population, not only because of distinct underlying mechanisms and clinical features of their heart disease, but also because of the potential ongoing need for additional cancer treatment as well as the altered duration of anticipated survival. In an effort to maximize both quality of life and survival, cardiologists and oncologists should collaborate with the aim of balancing the risks of cardiotoxicity with the benefits of oncologic therapy.
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PMID:Cardiotoxicity of anticancer treatments: what the cardiologist needs to know. 2084 80

Systemic sclerosis (SS) can involve the pericardium, myocardium, conduction system, and cardiac valves. The presence of overt clinical signs of cardiac disease is a poor prognostic sign. Clinical manifestations include dyspnea, palpitations, chest pain, syncope, and symptoms of right heart failure. Prevalence of clinically symptomatic pericardial disease is 5-16%. However, ecocardiographic prevalence is 5.4- 41% and at autopsy is 33-77.5%. Patchy fibrosis is the characteristic myocardial finding in SS. Contraction band necrosis is the typical pathological finding. Important complications of fibrosis include left ventricular hypertrophy, as well as systolic and diastolic dysfunction of both ventricles. Early detection of these abnormalities is very important, mainly of the diastolic dysfunction, since it occurs before the systolic dysfunction and can predict important cardiac damage. Association of skeletal myositis with myocardial disease has been described. Patients with skeletal myositis are more likely to develop congestive heart failure, sustained symptomatic arrythmias, and cardiac sudden death. Coronary arteries are normal in systemic sclerosis, but there is no endomyocardial vessel involvement. There is an increased prevalence of arrhytmias, mainly premature atrial and ventricular contractions, as well as conduction system disease. Cardiac valvular involvement is minor in systemic sclerosis; mitral valve is the most frequently affected. Other abnormalities described in this disease include peripheral large vessels stiffness and secondary cardiac involvement due to pulmonary and systemic arterial hypertension. Cardiac involvement confers a high morbi-mortality risk in systemic sclerosis.
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PMID:[Cardiac involvement in systemic sclerosis]. 2179 85

Breast cancer is commonly diagnosed in postmenopausal women, the majority of whom express 1 or more cardiovascular disease risk factors. Cardiovascular disease poses a significant competing risk for morbidity and mortality among nonmetastatic breast cancer survivors. Adjuvant systemic therapies may result in late-cardiac toxicity decades after treatment completion. The cumulative incidence of treatment-related cardiotoxic outcomes may be as high as 33% after some adjuvant breast cancer therapies. Breast cancer treatment-induced cardiotoxicity may manifest as cardiomyopathy, coronary ischemia, thromboembolism, arrhythmias and conduction abnormalities, and valvular and pericardial disease. Evidence indicates that preexisting cardiovascular conditions such as hypertension or left ventricular dysfunction may compound the adverse effects of cardiotoxic treatments. There are currently no published clinical practice guidelines that address ongoing cardiac surveillance for cardiotoxicity after breast cancer, and existing guidelines for monitoring and promoting cardiovascular health in older women are often not followed. The multidisciplinary prospective surveillance system proposed elsewhere in this supplement would allow for earlier detection of cardiotoxicity from treatment and may improve monitoring of cardiovascular health in the growing population of breast cancer survivors.
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PMID:Prospective surveillance and management of cardiac toxicity and health in breast cancer survivors. 2248 1

The cardiovascular impact of cancer therapies on the heart is one of the major concerns in the long-term follow-up of childhood cancer survivors (CCSs). Long-term cardiovascular effects include the development of left ventricular dysfunction resulting in congestive heart failure and ischemic heart disease, as well as valvular and pericardial disease. This is mainly ascribed to the cardiotoxic side effects of chemotherapeutic agents (especially anthracyclines) and radiotherapy, but other factors such as radiation and inflammation play a role in the effect of childhood cancer on the cardiovascular health. The most concerning effect is the high incidence of symptomatic heart failure in CCS patients treated with anthracyclines. More than 50 % of CCSs treated with anthracyclines develop asymptomatic left ventricular dysfunction after cancer therapy, with approximately 5 % developing clinical signs of heart failure during long-term follow-up. Once CCS patients develop congestive heart failure, prognosis is poor and is not influenced by current medical treatment strategies. To reduce the long-term burden of cardiovascular disease in pediatric cancer patients, a diversified approach will be necessary. In the acute phase, prevention of cardiac damage through the use of cardioprotective agents (e.g., dexrazoxane) or by administering less cardiotoxic chemotherapeutic agents is to be considered. A recent randomized trial suggested that the use of dexrazoxane reduced cardiac toxicity without affecting cancer outcomes. Especially patients requiring high doses of chemotherapeutic agents could benefit from this approach. Recent data suggest that genetic testing might identify patients at higher risk for cardiotoxicity. This seems mainly related to genes involved in drug metabolism. This would allow personalized approach adjusting chemotherapy based on cardiovascular risk profiling. This could be combined with newer monitoring strategies in the acute phase using newer echocardiographic techniques and biomarker screening to identify patients with early damage to the myocardium. For the long-term CCS cohort, early detection and treatment of early dysfunction prior to the development of congestive heart failure could potentially improve long-term outcomes. Promoting healthy lifestyles and controlling additional cardiovascular risk factors (e.g., obesity, diabetes, arterial hypertension) is an important task for every physician involved in the care of this growing cohort.
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PMID:Educational paper: decreasing the burden of cardiovascular disease in childhood cancer survivors: an update for the pediatrician. 2336 62

Cardiotoxicity is one of the most significant adverse effects of cancer treatment, and is responsible for considerable morbidity and mortality. Among the effects of chemotherapeutic agents on the cardiovascular system, the most frequent and serious is heart failure with ventricular systolic dysfunction. Other toxic effects include hypertension, thromboembolic disease, pericardial disease, arrhythmias and myocardial ischemia. For several decades, cancer therapy-induced cardiomyopathy was almost exclusively associated with the use of cumulative doses of anthracyclines, which cause permanent damage at the cellular level. However, new therapeutic agents, such as the monoclonal antibody trastuzumab, induce transient reversible myocyte dysfunction which is unrelated to the dose used. Early identification of potential cardiovascular injury, accurate diagnosis of cardiotoxic events and implementation of appropriate monitoring plans are essential in patients with cancer. Close cooperation between cardiologists and oncologists is thus crucial, in order to balance the risks and benefits of cardiotoxic anticancer therapy. In this article we review the various responses to cardiotoxic cancer treatments and their relationship with the main antineoplastic drugs used in clinical practice. In addition, we discuss the main guidelines on detection and monitoring of cardiotoxicity in patients with cancer.
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PMID:Cardiotoxicity associated with cancer therapy: pathophysiology and prevention strategies. 2362 3


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