Herz
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One crucial goal of magnetic resonance imaging (MRI) in patients with coronary artery disease (CAD) is the characterization of myocardial microcirculation that reflects tissue supply much better than detection and quantification of a stenosis itself. PERFUSION: Myocardial perfusion is one important parameter of microcirculation and it is commonly detected by first-pass techniques using contrast agents (CA). Despite the quantification of perfusion it is an indispensable component of a comprehensive diagnosis to determine the perfusion reserve, which is believed a good indicator for viability of myocardium. However, most MRI techniques for perfusion imaging are Ca based and this implies a restricted reproducibility in humans. Beyond it, most first-pass techniques are qualitative and not quantitative. REGIONAL BLOOD VOLUME: Another parameter of microcirculation is the regional intracapillary myocardial blood volume (RBV) that almost represents the whole intramyocardial blood volume due to its dominating volume fraction. The RBV reflects the autoregulatory adaptation of microvessels, e.g., a severe stenosis may lead to an increase of the RBV by capillary recruitment, and the RBV is reduced in scar areas. The RBV may be quantified by first-pass techniques; however, this demands a definite relation between signal intensity and concentration of the CA, which is difficult to find for the range of concentrations present during the first pass. Until recently, no techniques existed for the exact and noninvasive assessment of the RBV. CAPILLARY RECRUITMENT: The evaluation of the relevance of a coronary artery stenosis is of paramount interest for the therapeutic decision. A severe stenosis implies the activation of compensation mechanisms, which includes poststenotic dilation of the microvascular system. This lowering of the vascular resistance aims to maintain sufficient blood supply at least under resting conditions. However, many obstacles hamper the noninvasive assessment of this autoregulatory response so far. Our laboratory recently developed different techniques for the assessment of myocardial perfusion, regional myocardial blood volume, and capillary recruitment. These techniques are based on theoretical and physiologic considerations and work mainly without CA. In this article, feasibility and reproducibility of these approaches are shown in volunteers and patients. ⋯ We anticipated that poststenotic vasodilatation implies a capillary recruitment. Almost all (i.e., > 90%) of intramyocardial blood residues in that type of vessel. Due to their large arteriovenous oxygenation difference, myocardial capillaries contain considerable amounts of deoxyhemoglobin (Figure 3). Hence, in regions with autoregulatory capillary recruitment the tissue concentration of deoxyhemoglobin should be elevated when compared to myocardium supplied by a normal vessel (Figure 5b). Due to its paramagnetic property and its intravascular confinement, the natural CA deoxyhemoglobin may be assessed by susceptibility sensitive, or also called blood oxygenation level-dependent (BOLD) MRI. For T2* measurements, a segmented gradient echo pulse sequence was used, which acquired ten successive gradient echoes per rf excitation in a single breathhold. In volunteers, there was an increase in T2* of about 10% under dipyridamole-induced stress (Figure 4). This means a decrease of the intracapillary deoxyhemoglobin concentration, whereas the oxygen consumption under increased perfusion did not change. In myocardial regions of patients, associated with the stenotic artery T2* was significantly lower than in residual myocardium (p < 0.01; Figure 5a). This difference in T2* increased after application of the vasodilator dipyridamole (p < 0.001). In patients being reinvestigated after therapeutic interventions, the microvascular dilation was partly removed (Figure 5c). For the first time we could show that myocardial BOLD MRI detects poststenotic capillary recruitment dependent on a coronary artery stenosis.
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Randomized Controlled Trial Multicenter Study Clinical Trial
Colchicine for the prevention of postpericardiotomy syndrome.
Postpericardiotomy syndrome (PPS) is a troublesome complication of cardiac surgery, occurring in 10-45% of cases. Accepted modalities of treatment include nonsteroidal anti-inflammatory drugs, corticosteroids, and pericardiectomy in severe cases. The optimal method for prevention of PPS has not been established. Recent trial data have shown that colchicine is efficient in the secondary prevention of recurrent episodes of pericarditis. The aim of the present study was to evaluate the possible benefit of colchicine for the primary prevention of PPS in patients after cardiac surgery. To the best of our knowledge, this is the first study addressing this issue. ⋯ Colchicine may be efficacious for the prevention of PPS in patients after cardiac surgery. Further evaluations in larger clinical trials are warranted.
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Despite routine use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and spironolactone in patients with heart failure due to dilated cardiomyopathy (DCM), these patients still have a considerable annual mortality rate of 5-10%. Sudden unexpected death accounts for up to 50% of all deaths and is most often due to rapid ventricular tachycardia or ventricular fibrillation and less often due to bradyarrhythmias or asystole. ⋯ This review describes potential arrhythmia mechanisms in DCM and summarizes the results of antiarrhythmic drug trials and of prophylactic ICD trials in patients with heart failure as well as our knowledge concerning arrhythmia risk stratification in patients with DCM.
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Inherited ventricular arrhythmias such as the long QT syndrome (LQTS), Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT), idiopathic ventricular fibrillation (VF), and arrhythmogenic right ventricular cardiomyopathy (ARVC) account for a relevant proportion of sudden cardiac death cases in young patients cohorts. The detailed pathogenetic mechanisms of inherited ventricular arrhythmias are still poorly understood because systematic investigations are difficult to perform due to low patient numbers and the lack of appropriate experimental models. However, recent advances in research and science have identified a genetic background for many of these diseases. ⋯ This review summarizes the current knowledge of the molecular mechanisms, including aspects of pathoanatomy, autonomic innervation, genetics, and genotype-phenotype correlations with their potential implications for diagnosis and treatment of inherited ventricular arrhythmias.