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Three-dimensional (3D) echocardiographic imaging has been introduced as a tool to improve the assessment of both morphologic and functional parameters of the cardiovascular system. In the past, data acquisition was limited due to time-consuming sequential acquisition of multiple triggered 2D image planes from 10-60 heart cycles using transesophageal rotational, transthoracic rotational or transthoracic freehand approaches. Recent improvements in the size of matrix array probes and in computing power of modern ultrasound equipment have significantly increased both spatial and temporal resolution of "second-generation" real-time 3D scanners. Although the superiority of 3D echocardiography in the determination of ventricular volume, ventricular mass or valvular orifice area had already been demonstrated in the late 1990s, widespread use in clinical cardiology was limited on account of difficulties in acquisition and post-processing. Clinical use of modern 3D echocardiography is boosted by the marked reduction in acquisition time and the unique possibility of on-line rendering on the ultrasound system. The ability to visualize a virtual 3D surface in real time-although limited to a sector size of about 30 degrees-offers new insights into cardiac pathomorpholgy even in patients with arrhythmias and may in realtime 3D-contrast flow analysis. Analysis of wide-angle 3D datasets (90 by 90 degree pyramidal shape) is possible by combining the 3D information of several [4-7] consecutive heart cycles. 3D datasets including the complete left ventricle provide comprehensive information on ventricular and mitral valve morphology and function. Qualitative and quantitative analyses of regional wall motion at rest and during stress become possible. Combination with 3D color Doppler data allows additional assessment of valvular function as well as determination of flow in the left ventricular outflow tract and across septal defects. The integration and future quantification of these new parameters together with on-line review allows new insights into cardiac function, morphology and synchrony that offer great potentials in the evaluation of right and left ventricular global and regional function, diagnosis of small areas of ischemia, congenital and valvular heart disease and effects of biventricular pacing in dilated heart asynchrony.
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PMID:Second-generation real-time three-dimensional echocardiography. Finally on its way into clinical cardiology? 1508 67

A total of 265 patients suffering from infective endocarditis (IE) were operated on at the Center of Cardiology and Cardiovascular Surgery. Of these, 20 patients presented with arterial embolism of the peripheral arteries of varying standing (from in-hospital episodes of embolism to 8 months). Embolism of the cerebral arteries was identified in 8 (3.0%) patients with IE. In 5 patients, an embolus was located in the orifice of the internal carotid artery. Three persons were diagnosed to have embolism of the intracranial arteries. Thromboembolism of the limb arteries was present in 12 (4.5%) cases. Active IE was diagnosed in 11 patients; in 9 cases, IE was in a stage of remission, Bivalvular mitralaortic disease was present in 4 patients; aortic disease was identified in 9 and mitral disease in 7 patients. In 3 patients with acute disorders of cerebral circulation arising from embolism of the carotid arteries and in 3 patients with progressive acute limb ischemia due to embolism of lower limb arteries, the operations were performed on an emergency basis. In these cases, two stage operations were undertaken. Five patients presenting with infective aneurysms of lower limb arteries and thromboembolism of the peripheral arteries with chronic lower limb artery ischemia underwent one stage operations. The first stage of operation consisted in resection of the infected vascular segment and an aneurysm, the second stage in correction of valvular heart disease. The outcomes of operations were regarded as satisfactory in all the cases. No complications or lethal outcomes were recorded in the postoperative period.
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PMID:Surgery of arterial embolism in patients with infective endocarditis. 1562

Ischemic heart disease is the most common cause of mortality worldwide. Cardiac fibroblasts and myofibroblasts, i.e., the hypersecretory, muscular, and contractile fibroblastic phenotype variant, play an important role in myocardial healing and are responsible for accumulation of collagen in the infarct scar as well as in viable myocardium. Thus, cardiac fibroblasts and myofibroblasts directly contribute to cardiac stiffness, altered performance, and ultimately to the onset of systolic and diastolic heart failure. Cardiotrophin-1 (CT-1) is a member of the IL-6 superfamily and is elevated in the serum of patients with ischemic heart disease and valvular heart disease; it is also known to induce cardiomyocyte hypertrophy in vitro. The recent, burgeoning awareness of the functions of IL-6 superfamily of cytokines within cardiovascular diseases predicates this summary of CT-1's effect in cardiac wound healing, and particularly after the induction of myocardial infarction. Further, we summarize recent results of cardiac CT-1 expression post-myocardial infarction (post-MI) as well as the effect of CT-1 on cultured primary adult rat cardiac fibroblasts with respect to proliferation and collagen secretion. It would appear that CT-1 plays an important and heretofore largely unrecognized role in infarct scar formation and angiogenesis in the rat model of chronic MI. Further work is required to determine factors that induce CT-1 expression, its interplay with other mediators of cardiac infarct wound healing in the setting of acute cardiac ischemia and chronic post-MI heart failure, and ultimately whether it confers a beneficial effect or contributes to maladaptive cardiac fibrosis.
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PMID:Emerging evidence for the role of cardiotrophin-1 in cardiac repair in the infarcted heart. 1572 58

The clinical role of magnetic resonance in diseases of the heart and great vessels is rapidly evolving. Cardiovascular magnetic resonance (CMR) has become an established non-invasive imaging modality for the assessment of various cardiac disorders, such as congenital heart disease, cardiac masses, cardiomyopathies, aortic and pericardial diseases. Moreover, due to its accuracy and reproducibility, CMR is currently considered the gold standard for quantification of ventricular volumes, function, and mass. Thus, this technique is ideally suited to assess the efficacy of therapeutic interventions on ventricular hypertrophy and remodelling, which may allow a reduction in sample size to show clinically relevant effects. Comprehensive functional assessment is possible by CMR due to its capability to measure flow velocity and flow volume, which is a basic requirement to quantify lesion severity in valvular heart disease. Within the past years, major technical advances have considerably improved acquisition speed and image quality making CMR a useful tool for the evaluation of patients with ischaemic heart disease. Although the clinical robustness of coronary magnetic resonance angiography still needs improvement, CMR currently provides valuable information to detect reversible ischemia, myocardial infarction, and residual viability. In this review we will present in detail the well-established indications of CMR accompanied by an outlook on new applications that are likely to enter the clinical arena in the near future.
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PMID:Clinical applications of cardiovascular magnetic resonance. 1572 65

Three-dimensional (3-D) echocardiography has been an important research goal ever since the introduction of two-dimensional (2-D) echocardiography. Most approaches towards 3-D echocardiography were off-line and based on the sequential rotational scanning and acquisition of multiple cross-sectional images together with external or internal reference systems. These approaches were limited by long acquisition and analysis time in combination with poor image quality. Recently, improvements in the matrix array technology have significantly increased spatial and temporal resolution of second-generation real-time 3-D transducers. Clinical use of modern 3-D echocardiography is boosted by the marked reduction in acquisition time and the unique possibility of on-line rendering on the ultrasound system. The integration and future quantification of new parameters together with on-line review allows new insights into cardiac function, morphology and synchrony that offer great potentials in the evaluation of right and left global and regional function, diagnosis of small areas of ischemia, congenital and valvular heart disease and effects of biventricular pacing in dilated heart asynchrony. This report will review current and future applications of 3-D data acquisition, emphasizing the real-time methods and clinical applications of the new matrix array transducer.
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PMID:Three-dimensional echocardiography. 1600 52

Patients with diastolic heart failure (HF), i.e., clinical HF with normal or near normal left ventricular ejection fraction (LVEF), may develop unstable angina pectoris (UAP) due to epicardial atherosclerotic coronary artery disease and/or to subendocardial ischemia, even in the absence of coronary artery disease. However, the risk of UAP in ambulatory patients with diastolic HF has not been well studied. We examined incident hospitalizations due to UAP in 916 patients with diastolic HF (LVEF >45%) without significant valvular heart disease and 6,800 patients with systolic HF (LVEF <or=45%) in the Digitalis Investigation Group trial. During a 38-month median follow-up, 12% of patients (797 of 6,800) with systolic HF (incidence rate 435 per 10,000 person-years) and 15% of patients (138 of 916) with diastolic HF (incidence rate 536 per 10,000 person-years) were hospitalized for UAP (adjusted hazard ratio for diastolic HF 1.22, 95% confidence interval [CI] 1.02 to 1.47, p = 0.032). There was a graded increase in incident hospital admissions for UAP with increasing LVEF. Hospitalizations for UAP occurred in 11% (520 of 4,808, incidence rate 407 per 10,000 person-years), 14% (355 of 2,556, incidence rate 496 per 10,000 person-years), and 17% (60 of 352, incidence rate 613 per 10,000 person-years) of patients with HF, respectively, with LVEF values <35%, 35% to 55%, and >55%. Compared with patients with HF and an LVEF <35%, the adjusted hazard ratios for UAP hospitalization in those with LVEF values 35% to 55% and >55% were, respectively, 1.17 (95% CI 1.02 to 1.34, p = 0.028) and 1.57 (95% CI 1.20 to 2.07, p = 0.026). In conclusion, in ambulatory patients with chronic HF, a higher LVEF was associated with increased risk of hospitalizations due to UAP. As in patients with systolic HF, those with diastolic HF should be routinely evaluated for myocardial ischemia and managed accordingly.
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PMID:Hospitalizations due to unstable angina pectoris in diastolic and systolic heart failure. 1729 84

Many patients with acute heart failure have marked hypertension and preserved left ventricular ejection fraction. In these patients, the heart failure usually does not result from transient systolic dysfunction or valvular abnormalities but rather results from diastolic dysfunction. Treatment of this condition includes control of hypertension, cautious diuresis, and, if necessary, ventilatory support. Further workup after the acute phase should be directed by the overall clinical picture. Other potential contributing factors, such as renal artery stenosis, valvular heart disease, and ischemia, should be strongly considered. Unfortunately, chronic therapy for diastolic heart failure has not yet been standardized due to the paucity of clinical trial data. Strict control of hypertension appears to be of paramount importance. Angiotensin-converting enzyme inhibitors or receptor blockers may be of benefit in preventing repeat hospitalizations.
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PMID:Acute heart failure with preserved systolic function. 1815 78

Flash pulmonary edema (FPE) is a general clinical term used to describe a particularly dramatic form of acute decompensated heart failure. Well-established risk factors for heart failure such as hypertension, coronary ischemia, valvular heart disease, and diastolic dysfunction are associated with acute decompensated heart failure as well as with FPE. However, endothelial dysfunction possibly secondary to an excessive activity of renin-angiotensin-aldosterone system, impaired nitric oxide synthesis, increased endothelin levels, and/or excessive circulating catecholamines may cause excessive pulmonary capillary permeability and facilitate FPE formation. Renal artery stenosis particularly when bilateral has been identified has a common cause of FPE. Lack of diurnal variation in blood pressure and a widened pulse pressure have been identified as risk factors for FPE. This review is an attempt to delineate clinical and pathophysiological mechanisms responsible for FPE and to distinguish pathophysiologic, clinical, and therapeutic aspects of FPE from those of acute decompensated heart failure.
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PMID:Flash pulmonary edema. 1991 37

Cardiotrophin (CT)-1 was discovered by coupling expression cloning with an embryonic stem cell-based model of cardiogenesis. Comparison of similarity in amino acid sequence and conformational structure indicates that CT-1 is a member of the interleukin (IL)-6 type cytokine family that shares the transmembrane signaling protein, glycoprotein (gp) 130 as a receptor. These cytokines mediate overlapping pleiotropic actions on a variety of cell types including cardiac myocytes, hepatocytes, megakaryocytes, osteoclasts, and neuronal cells. CT-lmediates its hypertrophic and cytoprotective properties through the Janus kinase/signal transducers and activators of transcription (JAK/STAT), mitogen-activated protein (MAP) kinase, phosphatidylinositol (PI) 3 kinase, and nuclear factor kappa B (NFkappaB) pathways. CT-1 gene and protein are distributed not only in the heart, but also in the pulmonary, renal, gastrointestinal, cerebral, and muscular tissues. CT-1 could also be synthesized and secreted from vascular endothelial cells and adipocytes. CT-1 has hypertrophic actions on the cardiac myocytes, skeletal muscle cells, and smooth muscle cells as well as cytoprotective actions on the cardiac myocytes, neuronal cells, and hepatocytes. CT-1 is circulating in the body, and its plasma concentration is increased in various cardiovascular and renal diseases such as hypertension, congestive heart failure, myocardial infarction, valvular heart disease, metabolic syndrome, and chronic kidney disease. Treatment with CT-1 is beneficial in experimental animal models of cardiovascular diseases. CT-1 specifically protects the cardiac myocytes from ischemic damage when CT-1 is given not only prior to the ischemia, but also given at the time of reoxygenation. Current evidence suggests that CT-1 plays an important role in the regulation of the cardiovascular system.
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PMID:Cardiotrophin-1 in cardiovascular regulation. 2127 39

Giant cell arteritis involving intramural coronary artery branches is rare, and its clinical features remain poorly understood. We report a 56-year-old hemodialysed patient with a history of mitral valve replacement, who presented with "fever of unknown origin" and intractable hypotension. The antemortem diagnosis was very difficult and the autopsy revealed giant-cell-rich vasculitis in arteries in multiple organs. The heart was most severely involved, in which almost all of the intramural coronary artery branches were infiltrated by many multinucleated giant cells, macrophages, and lymphocytes with luminal narrowing, but the epicardial segments of the coronary arteries were spared. Superimposed on the preexisting valvular heart disease, the vasculitic lesions were thought to play a central role in severe cardiac dysfunction resulting in dialysis-related hypotension, which led to fatal non-occlusive mesenteric ischemia. This case highlights the possibility that giant cell arteritis of intramural coronary arteries could be an uncommon underlying cause of refractory dialysis-related hypotension.
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PMID:Atypical giant cell arteritis predominantly involving intramural coronary arteries: a case showing refractory dialysis-related hypotension. 2165 3


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