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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carcinoid heart disease is a rare form of valvular heart disease. The management of these patients is complex, as the systemic malignant disease and the cardiac involvement have to be considered at the same time. Progress in the treatment of patients with carcinoid disease has resulted in improved symptom control and survival. Development and progression of carcinoid heart disease are associated with increased morbidity and mortality. In patients with severe cardiac involvement and well-controlled systemic disease, cardiac surgery has been recognized as the only effective treatment option. Valve replacement surgery may not only be beneficial in terms of symptom relief, but may also contribute to the improved survival observed over the past 2 decades in patients with carcinoid heart disease. Early diagnosis and early surgical treatment in appropriately selected patients may provide the best results. In this article, we review the current literature regarding the biology, diagnosis, treatment, and prognosis of carcinoid heart disease.
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PMID:Carcinoid heart disease. 1749 24

Atherosclerosis is a systemic disease responsible for strokes, myocardial infarction, renal hypertension, and intermittent claudication. Acute coronary syndromes (unstable angina, acute myocardial infarction, and sudden cardiac death) are the major causes of morbidity and mortality in developed countries. These acute manifestations of heart disease share a common pathophysiologic phenomenon: coronary thrombosis. Two principal mechanisms are responsible for coronary thrombosis: plaque disruption (75%) and plaque erosion (25%). Disrupted plaques exhibit a large lipid content, increased macrophages, and a thin fibrous cap. Hypercholesterolemia and diabetes are associated with plaque disruption. Eroded plaques are smooth muscle-cell rich with an intact fibrous cap. Cigarette smoking is associated with plaque erosion, most frequently in women with sudden death when they are younger than 50 years of age. Systemic inflammation is a novel, robust marker for future cardiovascular events, not only in patients with established atherosclerotic disease but also in apparently healthy individuals. Local inflammation at the plaque disruption site is documented by increased macrophage infiltration. Macrophages are responsible for plaque disruption, neovascularization, smooth muscle cell apoptosis, and plaque thrombogenicity. Experimental studies have identified the lipid core as the most thrombogenic substrate of the atherosclerotic plaque. Tissue factor, a cell membrane-bound protein, is crucial in thrombus formation. Tissue factor is expressed in apoptotic macrophages, suggesting that macrophages are not only responsible for plaque disruption but also pivotal in thrombus generation, the most important mechanism of acute coronary syndromes.
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PMID:Pathophysiology of plaque disruption and thrombosis in acute ischemic syndromes. 1790 43

To this day the aetiology of sarcoidosis continues to elude definition. Partially as a consequence of this, little in the way of new therapies has evolved. The enigma of this condition is that, unusually for a disease with the potential for devastating consequences, many patients show spontaneous resolution and recover. Cardiac involvement can affect individuals of any age, gender or race and has a predilection for the conduction system of the heart. Heart involvement can also cause a dilated cardiomyopathy with consequent progressive heart failure. The most common presentation of this systemic disease is with pulmonary infiltration, but many cases will be asymptomatic and are detected on routine chest radiography revealing lymphadenopathy. Current advances lie in the newer methods of imaging and diagnosing this unusual heart disease. This review describes the pathology and diagnosis of this condition and the newer imaging techniques that have developed for determining cardiac involvement.
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PMID:Sarcoid heart disease. 1791 69

Pulmonary hypertension (PH) is a hemodynamic state characterized by elevation in the mean pulmonary arterial pressure and pulmonary vascular resistance leading to right ventricular failure and premature death. PH can be the result of a variety of diseases of different etiologies. Pulmonary arterial hypertension (PAH) should be distinctly differentiated from pulmonary venous hypertension (PVH) as a result of left heart disease. PAH is commonly caused by or associated with an underlying pulmonary, cardiac, or systemic disease (APAH). In the absence of an identifiable etiology or associated underlying disease, PAH is referred to as idiopathic (IPAH). IPAH, formerly known as primary pulmonary hypertension (PPH), is a rare disease most commonly seen in women of childbearing age. Presenting symptoms and signs are nonspecific and include dyspnea on exertion, fatigue, and a loud pulmonary component of the second heart sound. Transthoracic Doppler echocardiography is an excellent noninvasive test to detect the presence of pulmonary hypertension, although every patient should receive a right heart catheterization to confirm the diagnosis. A detailed work up, including laboratory tests and imaging studies, is also indicated to rule out known causes of pulmonary hypertension. Several targeted treatment options have become available in recent years and include parenteral and inhaled prostanoids, oral endothelin receptor antagonists, and oral phosphodiesterase type-5 inhibitors. As a result of their complex care, patients should be referred to centers with expertise in pulmonary hypertension.
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PMID:Pulmonary hypertension: evaluation and management. 1800 30

In patients with carcinoid heart disease, a multidisciplinary approach to patient care is required because treatment of the systemic disease and management of cardiac involvement must be considered at the same time. Somatostatin analogue use is a therapeutic cornerstone, effective in symptomatic control of the endocrine syndrome. Chemotherapy is of limited efficacy in patients with carcinoid tumors. Hepatic resection of metastases is the preferred treatment option and has been shown to result in improved outcome. It should be considered if at least 90% of the metastases in the liver are removable. Hepatic artery embolization is usually applied if a patient is not eligible for surgical debulking. Development and progression of carcinoid heart disease complicate the carcinoid syndrome and contribute to poor prognosis. In patients with severe cardiac involvement and well-controlled systemic disease, valve replacement surgery is an effective treatment modality that can relieve intractable symptoms and contribute to improved outcome.
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PMID:Carcinoid heart disease. 1822

Several reports have demonstrated an association between psoriasis and cardiovascular diseases such as hypertension, valvular disease and arrhythmia. However, the data is scarce. Forty-seven psoriasis patients and 20 healthy people underwent transthoracic echocardiographic examination including pulse- and tissue Doppler analysis and 24-h ambulatory electrocardiographic monitoring including heart rate variability (HRV) analysis. Patients having systemic hypertension, diabetes mellitus, history of structural or ischemic heart disease, chronic obstructive pulmonary disease and any associated systemic disease were excluded. Psoriasis Area and Severity Index (PASI) was calculated and severe psoriasis was defined in the case of history of hospitalizations for psoriasis and/or getting systemic therapy. Mean age of the patients was 35.7 +/- 12.9 years and disease duration was 123.2 +/- 84.3 (3-360) months. PASI ranged from 0.4 to 34.0 (mean +/- SD: 7.1 +/- 6.6) and 20 (42.6%) patients had severe psoriasis. There were no significant differences between psoriasis patients and control group with respect to mean values of blood pressure, body mass index, lipid profile and cardiac dimensions. However, frequency of being overweight was significantly higher in psoriasis patients (42.6 vs. 10.0%, P = 0.011). No patient had valvular disease. Mild pulmonary hypertension (PH) (30-40 mmHg) was significantly more frequent in psoriasis patients (31.9 vs. 0%, P = 0.003). Pulse wave mitral Doppler deceleration and isovolumetric relaxation times were significantly longer in psoriasis patients (195.9 +/- 29.7 vs. 191.6 +/- 14.7 ms, P = 0.002 and 91.6 +/- 14.7 vs. 79.6 +/- 10.5 ms, P = 0.001, respectively). However, frequency of diastolic dysfunction was not significantly different than the control group (8.5 vs. 0%, P = 0.309). HRV parameters and frequency of supraventricular and ventricular premature beats were not significantly different between the groups. No patient had ventricular tachycardia. Echocardiographic follow-up of psoriasis patients may be important due to possible association of PH. However, incidences of structural heart disease and arrythmia are not increased in psoriasis according to our results.
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PMID:Increased frequency of pulmonary hypertension in psoriasis patients. 1844 54

Heart diseases resulting in heart failure are among the leading causes of morbidity and mortality in the Western world and can result from either systemic disease (e.g., hypertensive heart disease, ischemic heart disease) or specific heart muscle disease (e.g., dilated cardiomyopathy/DCM). Subproteome analysis of such disease subsets affords a reduction in sample complexity, potentially revealing biomarkers of cardiac failure that would otherwise remain undiscovered in proteome wide studies. Label-free nanoscale LC-MS has been applied in this study to validate a Triton X-114-based phase enrichment method for cardiac membrane proteins. Annotation of the subcellular location combined with GRAVY score analysis indicates a clear separation between soluble and membrane-bound proteins with an enrichment of over 62% for this protein subset. LC-MS allowed confident identification and annotation of hydrophobic proteins in this control sample pilot study and demonstrates the power of the proposed technique to extract integral membrane-bound proteins. This approach should be applicable to a wider scale study of disease-associated changes in the cardiac membrane subproteome.
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PMID:Nonionic detergent phase extraction for the proteomic analysis of heart membrane proteins using label-free LC-MS. 1871 67

This case illustrates an unusual presentation of atrial fibrillation in a 10-year-old male neutered Maine coon. At the time of diagnosis of the arrhythmia the size of the left atrium determined by echocardiography was within normal limits and no structural or functional heart or other systemic disease was identified. Traditionally it has been suggested that the atria must be of a sufficient size in order to sustain atrial fibrillation (multiple wavelet theory) and therefore only cats with significant cardiac disease can attain sufficiently large atria to sustain this arrhythmia. To the author's knowledge this is the first detailed case report of sustained atrial fibrillation in a cat with a normal sized left atrium and no obvious structural heart disease seen on cardiac ultrasound.
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PMID:A case of sustained atrial fibrillation in a cat with a normal sized left atrium at the time of diagnosis. 1908 29

The term 'cardiorenal syndrome' (CRS) has increasingly been used in recent years without a constant meaning and a well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of the heart-kidney interactions, the classification of the CRS today includes 5 subtypes whose etymology reflects the primary and secondary pathology, the time frame and simultaneous cardiac and renal codysfunction secondary to systemic disease. The CRS can generally be defined as a pathophysiological disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness. The identification of patients and the pathophysiological mechanisms underlying each syndrome subtype will help to understand clinical derangements, to make the rationale for management strategies and to design future clinical trials with accurate selection and stratification of the studied population.
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PMID:The cardiorenal syndrome. 1916 27

The term cardiorenal syndrome (CRS) has increasingly been used in recent years without a constant meaning and a well accepted definition. To include the vast array of interrelated derangements, and to stress the bi-directional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome includes today five sub-types whose etymology reflects the primary and secondary pathology, the time-frame and simultaneous cardiac and renal co-dysfunction secondary to systemic disease. The cardiorenal syndrome can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Type I CRS reflects an abrupt worsening of cardiac function (e.g. acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type II CRS describes chronic abnormalities in cardiac function (e.g. chronic congestive heart failure) causing progressive and permanent chronic kidney disease. Type III CRS consists in an abrupt worsening of renal function (e.g. acute kidney ischaemia or glomerulonephritis) causing acute cardiac disorder (e.g. heart failure, arrhythmia, ischemia). Type IV CRS describes a state of chronic kidney disease (e.g. chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy and/or increased risk of adverse cardiovascular events. Type V CRS reflects a systemic condition (e.g. diabetes mellitus, sepsis) causing both cardiac and renal dysfunction. Biomarkers can help to characterize the subtypes of the CRS and to indicate treatment initiation and effectiveness.
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PMID:[Cardiorenal syndrome, current understanding]. 1955 20


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