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Myocardial Fibrosis (myocardial + fibrosis)
Selected AbstractsPatchy Myocardial Fibrosis 20 Years after Radiation TherapyECHOCARDIOGRAPHY, Issue 1 2007Rachael A. Wyman M.D. We describe a case of a young woman diagnosed with Ewings sarcoma at age 8 and treated with adriamycin and radiation therapy. Twenty years later the patient has a cardiomyopathy and a focal area of patchy infiltration of fibrotic tissue along the left ventricle and atrium. Although fibrosis due to radiation exposure has been demonstrated on biopsy and autopsy studies, we are not aware of previous reports of echocardiographic demonstration of this finding. The most likely explanation for the fibrosis location is the left posterolateral direction of the radiation beam. [source] Relationship between Left Ventricular Geometry and Left Ventricular Systolic and Diastolic Functions in Patients with Chronic Severe Aortic RegurgitationECHOCARDIOGRAPHY, Issue 6 2008Murat Çayli M.D. Background: Chronic aortic regurgitation (AR) is a form of volume overload inducing left ventricle (LV) dilatation. Myocardial fibrosis, apoptosis, progressive LV dilatation, and eventually LV dysfunction are seen with the progression of disease. The aim of the study was to assess the relation between LV geometry and LV systolic and diastolic functions in patients with chronic severe AR. Methods: The study population consisted of 88 patients with chronic severe AR and 42 healthy controls. The LV ejection fraction (LVEF) was calculated. Subjects were divided as Group I (controls, n = 42), Group II (LVEF > 50%, n = 47), and Group III (LVEF < 50%, n = 41). Transmitral early and late diastolic velocities and deceleration time were measured. The annular systolic (Sa) and diastolic (Ea and Aa) velocities were recorded. Diastolic function was classified as normal, impaired relaxation (IR), pseudonormalization (PN), and restrictive pattern (RP). Results: The LVEF was similar in Group I and II, while significantly lower in Group III. Sa velocity was progressively decreasing, but LV long- and short-axis diameters were increasing from Group I to Group III. Forty-six, 31 and 11 patients had IR, PN, and RP, respectively. LV long-axis systolic and diastolic diameters were significantly increasing, while LVEF and Sa velocity were significantly decreasing from patients with IR to patients with RP. The LV long-axis diastolic diameter is independently associated with LV systolic and diastolic functions. Conclusions: The LV long-axis diastolic diameter is closely related with LV systolic and diastolic functions in patients with chronic severe AR. [source] Mechanisms of Cardiac Fibrosis in HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 7 2007Javier Díez MD Changes in the composition of cardiac tissue develop in hypertensive patients with left ventricular hypertrophy (ie, hypertensive heart disease) and lead to structural remodeling of the myocardium. One of these changes is related to the disruption of the equilibrium between the synthesis and degradation of collagen types I and III molecules, which results in an excessive accumulation of collagen types I and III fibers within the myocardium. Myocardial fibrosis is the consequence of a number of pathologic processes mediated by mechanical, neurohormonal, and cytokine routes. The clinical relevance of fibrosis is that it may contribute to heart failure and other cardiac complications in patients with hypertensive heart disease. This brief review focuses on the mechanisms of hypertensive myocardial fibrosis. [source] Evaluation of Right Ventricular Fibrosis in Adult Congenital Heart Disease Using Gadolinium-enhanced Magnetic Resonance Imaging: Initial Experience in Patients with Right Ventricular Loading ConditionsCONGENITAL HEART DISEASE, Issue 5 2006Lopa P. Hartke MD ABSTRACT Objective., Gadolinium-enhanced cardiac magnetic resonance imaging has been used to show myocardial fibrosis, a finding that appears as late gadolinium enhancement. Its role in the evaluation of right ventricular fibrosis in congenital heart disease is unclear. The purpose of this study was to demonstrate late gadolinium enhancement of the right ventricle in adult and adolescent congenital heart disease and to investigate the relationship between this enhancement and clinical and pathophysiological data. Design., In total, 24 patients, 16 patients with congenital heart disease and right ventricular loading conditions and 8 controls, underwent gadolinium-enhanced viability imaging. Diagnoses varied and included repaired, palliated, and unrepaired lesions. The presence and extent of right ventricular late gadolinium enhancement was compared with patient clinical and hemodynamic data. Exact Wilcoxon tests, Fisher's exact tests, and Spearman's rank correlation were used to compare variables. Results., Nine of 16 patients (56%) were found to have right ventricular late gadolinium enhancement, ranging from 5% to 80% of right ventricular myocardium affected (mean 36.1%, SD 29.7). The combination of right ventricular systolic pressure ,98 mm Hg and systemic oxygen saturation ,93% strongly suggested the presence of right ventricular late gadolinium enhancement (positive predictive value 100%), but no single variable or combination of variables could reliably predict its absence (negative predictive values ,75%). Extent of right ventricular late gadolinium enhancement did not correlate with degree of either hypoxia or right ventricular hypertension. Conclusions., Gadolinium-enhanced cardiac magnetic resonance demonstrates right ventricular late gadolinium enhancement in some patients with congenital heart disease and right ventricular loading conditions. Clinical variables were associated with the presence of fibrosis but did not reliably predict severity. Myocardial preservation is likely a multifactorial process that may affect the right and left ventricles differently. [source] "Supranormal" Cardiac Function in Athletes Related to Better Arterial and Endothelial FunctionECHOCARDIOGRAPHY, Issue 6 2010Maria Florescu M.D. Objective: Athlete's heart is associated with left ventricular (LV) hypertrophy (LVH), and "supranormal" cardiac function, suggesting that this is a physiological process. Hypertrophy alone cannot explain increase in cardiac function, therefore, other mechanisms, such as better ventriculo-arterial coupling might be involved. Methods: We studied 60 male (21 ± 3 years) subjects: 27 endurance athletes, and a control group of 33 age-matched sedentary subjects. We assessed global systolic and diastolic LV function, short- and long-axis myocardial velocities, arterial structure and function and ventriculo-arterial coupling, endothelial function by flow-mediated dilatation, and amino-terminal pro-brain natriuretic peptide (NT-proBNP) and biological markers of myocardial fibrosis and of oxidative stress. Results: Athletes had "supranormal" LV longitudinal function (12.4 ± 1.0 vs 10.1 ± 1.4 cm/s for longitudinal systolic velocity, and 17.4 ± 2.6 vs 15.1 ± 2.4 cm/s for longitudinal early diastolic velocity, both P < 0.01), whereas ejection fraction and short-axis function were similar to controls. Meanwhile, they had better endothelial function (16.7 ± 7.0 vs 13.3 ± 5.3%, P < 0.05) and lower arterial stiffness (pulse wave velocity 7.1 ± 0.6 vs 8.8 ± 1.1 m/s, P = 0.0001), related to lower oxidative stress (0.259 ± 0.71 vs 0.428 ± 0.88 nmol/mL, P = 0.0001), with improved ventriculo-arterial coupling (37.1 ± 21.5 vs 15.5 ± 13.4 mmHg.m/s3× 103, P = 0.0001). NT-proBNP and markers of myocardial fibrosis were not different from controls. LV longitudinal function was directly related to ventriculo-arterial coupling, and inversely related to arterial stiffness and to oxidative stress. Conclusions: "Supranormal" cardiac function in athletes is due to better endothelial and arterial function, related to lower oxidative stress, with optimized ventriculo-arterial coupling; athlete's heart is purely a physiological phenomenon, associated with "supranormal" cardiac function, and there are no markers of myocardial fibrosis. (Echocardiography 2010;27:659-667) [source] Regional Diastolic and Systolic Function by Strain Rate Imaging for the Detection of Intramural Viability during Dobutamine Stress Echocardiography in a Porcine Model of Myocardial InfarctionECHOCARDIOGRAPHY, Issue 5 2010Carsten Schneider M.D. The aim of this study was to evaluate diastolic and systolic strain rate measurements for differentiation of transmural/nontransmural infarction during dobutamine stress echocardiography (DSE). An ameroid constrictor was placed around the circumflex artery in 23 pigs inducing chronic vessel occlusion. Five pigs without constrictor served as controls. During high-dose DSE systolic strain rates (SRsys), systolic and postsystolic strain values (,sys, ,ps) and early and late diastolic strain rates (SRE and SRA) were determined. At week 6, animals were evaluated regarding myocardial fibrosis. Histology revealed nontransmural in 14 and transmural infarction in 9 animals. In controls, dobutamine induced a linear increase of SRsys to 12.3 ± 0.4 s,1 at 40 ,g/kg per minute (P = 0.001) and a linear decrease of SRE to ,6.6 ± 0.3 s,1 (P = 0.001). In the nontransmural group, SRsys, ,sys, ,ps at rest, and during DSE were higher and SRE was lower than in the transmural infarction group (P = 0.01). Best predictors for viability were SRsys (ROC 0.96, P = 0.0003), SRE at 10 ,g/kg per minute dobutamine stimulation (ROC 0.94, P = 0.001) and positive SR values during isovolumetric relaxation at 40 ,g/kg per minute dobutamine (ROC 0.86, P = 0.004). The extension of fibrosis correlated with SRsys at rest, ,sys at rest, and SRE at rest (P < 0.001). For the detection of viability similar diagnostic accuracies of SRE and SRsys were seen (sensitivity 93%/93%, specificity 96%/94%, respectively). Diastolic SR analysis seems to be equipotent for the identification of viable myocardium in comparison to systolic SR parameters and allows the differentiation of nontransmural from transmural myocardial infarction with high diagnostic accuracy. (Echocardiography 2010;27:552-562) [source] Age Dependency of Myocardial Structure: A Quantitative Two-Dimensional Echocardiography Study in a Normal PopulationECHOCARDIOGRAPHY, Issue 3 2000MARIA-AURORA MORALES M.D. Histological changes of the myocardium occur with aging due to an increase in collagen content, hypertrophy of fibers, and patchy fibrosis. Quantitative analysis of conventional echocardiographic images provides an in vivo assessment of myocardial structure by the evaluation of the gray level distribution; with this technique, a relation between myocardial fibrosis and pathological ultrasonic response has been documented. The aim of this study was to evaluate the relation between ultrason-ically assessed myocardial structure and age in a normal population. Seventy-eight subjects (47 men; mean age, 51 years; age range, 23,87 years) without apparent cardiovascular and systemic disease underwent conventional two-dimensional echocardiographic examinations. Still frames at end-diastole from apical four-chamber view were digitized and converted in matrices of 256 × 256 pixels. First-order statistical analysis was performed to describe a region of interest in the interventricular septum. The following parameters were studied: mean (gray level amplitude), standard deviation (overall contrast), uniformity (tonal organization), and entropy (tendency of gray levels to be spread). Myocardial structure was assessed in 75 of 78 subjects, divided into three groups: I, age 23,40 years; II, age 41,65 years; and III, > 65 years. Significant differences for all the parameters were found between the age groups. Age correlated directly with mean and entropy (r = 0.77 and 0.69, respectively) and inversely with uniformity (r = 0.70). Our results suggest that quantitative echocardiography can reveal age-related changes in myocardial structure that are characterized by a greater echogenicity and loss in tonal organization, possibly due to increased collagen content within the fibers. [source] Use of morphine and 6-monoacetylmorphine in blood for the evaluation of possible risk factors for sudden death in 192 heroin usersADDICTION, Issue 4 2003Anna Fugelstad Abstract Aims, To detect risk factors for sudden death from heroin injection. Design, Evaluation of data from forensic investigations of all fatal cases of suspected heroin death in a metropolitan area. Only cases with detectable morphine and 6-monoacetylmorphine (6-MAM) in blood were included in order to select heroin intoxication cases. Setting, Stockholm, Sweden. Measurements, Autopsy investigation and toxicological analysis of blood and urine; and police reports. Findings, In two-thirds of the 192 cases, death occurred in public places, and mostly without any time delay. Blood concentrations of morphine ranged from 50 to 1200 ng/g, and of 6-MAM from 1 to 80 ng/g. Codeine was detected in 96% of the subjects. In the majority of cases the forensic investigation indicated polydrug use, the most common additional findings being alcohol and benzodiazepines. However, in one-quarter of the cases other drug combinations were found. Previous abstinence from heroin and use of alcohol were identified as risk factors. For 6-MAM there was also a correlation with the presence of THC and benzodiazepines. Despite a high frequency of heart abnormalities (e.g. myocarditis and focal myocardial fibrosis), these conditions did not correlate with morphine or 6-MAM blood concentrations. Conclusions, We confirm that alcohol intake and loss of tolerance are risk factors for death from heroin use, whereas no connection to heart pathology was observed. Further, prospective, studies should focus on other possible risk factors. [source] Tissue inhibitor of metalloproteinse-1 is a marker of diastolic dysfunction using tissue doppler in patients with type 2 diabetes and hypertensionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2005M. H. Tayebjee Abstract Background, Tissue inhibitor of metalloproteinase-1 (TIMP-1) is associated with increased fibrosis of the extracellular matrix (ECM). Myocardial stiffness is a feature of diastolic dysfunction. We assessed circulating TIMP-1 as a marker of diastolic dysfunction in patients with type 2 diabetes mellitus (DM) and hypertension, who were compared with healthy controls. Methods, We recruited 54 patients (43 males; mean age 68 ± 5 years) with treated type 2 DM (i.e. controlled glycaemia, hypertension, hyperlipidaemia), 35 (30 males; 69 ± 8 years) treated nondiabetic hypertensives, and 31 healthy controls (18 males; 66 ± 5 years). Circulating TIMP-1 was measured by ELISA. Using transthoracic echocardiography, the early (E) diastolic mitral inflow velocity was measured with pulse wave Doppler, and the early mitral annular velocity (e,), a recognized index of diastolic relaxation, was measured with tissue Doppler. The E/A ratio was also calculated and isovolumic relaxation time measured. Results, Mean e, levels differed significantly between controls, diabetics and hypertensives (P < 0·0001). Circulating TIMP-1 was significantly different between patients and controls (P = 0·006), but there was no statistically significant difference between the DM and hypertension group. In both groups, only e, was negatively correlated with TIMP-1 levels, with a stronger correlation among the hypertensive patients (Spearman r = ,0·544, P = 0·001) when compared with the diabetic group (r = ,0·341, P = 0·011). Conclusion, Diastolic relaxation is impaired in diabetes and hypertensive patients. The relationship between TIMP-1 and e, may reflect increased myocardial fibrosis and consequent diastolic dysfunction, which may be more prominent in hypertension. [source] Cardiac L-type calcium current is increased in a model of hyperaldosteronism in the ratEXPERIMENTAL PHYSIOLOGY, Issue 6 2009Beatriz Martin-Fernandez Accumulating evidence supports the importance of aldosterone as an independent risk factor in the pathophysiology of cardiovascular disease. It has been postulated that aldosterone could contribute to ventricular arrhythmogeneity by modulation of cardiac ionic channels. The aim of this study was to analyse ex vivo the electrophysiological characteristics of the L-type cardiac calcium current (ICaL) in a model of hyperaldosteronism in the rat. Aldosterone was administered for 3 weeks, and cardiac collagen deposition and haemodynamic parameters were analysed. In addition, RT-PCR and patch-clamp techniques were applied to study cardiac L-type Ca2+ channels in isolated cardiomyocytes. Administration of aldosterone induced maladaptive cardiac remodelling that was related to increased collagen deposition, diastolic dysfunction and cardiac hypertrophy. In addition, ventricular myocytes isolated from the aldosterone-treated group showed increased ICaL density and conductance and prolongation of the action potential duration. No changes in kinetics or in voltage dependence of activation and inactivation of ICaL were observed, but relative expression of CaV1.2 mRNA levels was higher in cardiomyocytes isolated from the aldosterone-treated group. The present study demonstrates that aldosterone treatment induces myocardial fibrosis, cardiac hypertrophy, increase of ICaL density, upregulation of L-type Ca2+ channels and prolongation of action potential duration. It could be proposed that aldosterone, through these mechanisms, might exert pro-arrhythmic effects in the pathological heart. [source] Mitral Regurgitation After Partial Left Ventriculectomy As the Cause of Ventricular RedilatationJOURNAL OF CARDIAC SURGERY, Issue 2 2001Akira T. Kawaguchi M.D. Background: It remains unclear whether ventricular redilatation after partial left ventriculectomy (PLV) is due to underlying pathology or to continued volume overload amenable to surgery. Methods: Among patients undergoing PLV, 32 had Doppler echocardiography preoperatively, immediately after surgery (> 1 week), early after surgery (1,3 months), and late after surgery (8,14 months). Patients were divided into groups with mitral regurgitation (MR; MR+, n = 16) and without postoperative MR (MR-, n = 16) and were compared for ventricular size, performance, and survival. Results: After initial surgical reduction, left ventricular dimension on average gradually increased back to the preoperative level in subgroups of patients with valvular disease and cardiomyopathy and in all patients combined. Most patients showed drastically reduced left ventricular dimension early after PLV. In MR+ patients, dimension increased back to the preoperative level within 3 months after surgery, whereas the MR- group maintained reduced dimension throughout the first year in all patients combined and in a subgroup of patients with cardiomyopathy. Occurrence of significant MR after PLV appeared to be related to severity of fibrosis in excised myocardium but not to severity of preexisting MR, etiology, or performance of mitral valvuloplasty. Conclusions: Early postoperative MR, residual or new, appeared to play an important role in dictating early hemodynamics and late outcome in patients undergoing PLV. Results suggest an aggressive simultaneous approach to abolish MR. Causative role of myocardial fibrosis remains unclear and needs further study. [source] Aortic Dissection and Third-Degree Atrioventricular Block in a Patient With a Hypertensive CrisisJOURNAL OF CLINICAL HYPERTENSION, Issue 1 2008Nikolaos Lionakis MD A 55-year-old man with a history of uncontrolled hypertension was admitted because of an episode of severely elevated blood pressure. An electrocardiogram revealed complete atrioventricular block while imaging showed a dissecting aneurysm of the descending thoracic and abdominal aorta, type B according to the Stanford classification. Laboratory tests revealed significant increases in serum C-reactive protein. Coronary arteriography was performed and was negative for coronary artery disease. A VDD pacemaker was placed, and a combination of 4 antihypertensive agents was used as treatment. Type B aortic dissection may present with a wide range of manifestations. The authors suggest that measurement of C-reactive protein may be used in hypertensive patients to help reflect vascular injury and its degree, progression, and prognosis. Disorders of intraventricular conductivity are rarely seen in both types of dissection of the aorta (type A, B). Atrioventricular conductivity disorders that result in complete atrioventricular block have been reported only in patients with type A dissection (before the bifurcation of the subclavian artery). In this particular case, however, the authors diagnosed an atrioventricular conductivity disorder causing atrioventricular block in a patient with type B dissection. Consequently, the authors speculate that myocardial fibrosis, as a result of long-standing hypertension, could be the main pathogenetic mechanism leading to the development of such phenomena, resulting from a potential expanding of the fibrotic process to the atrioventricular conduction system. [source] Mechanisms of Cardiac Fibrosis in HypertensionJOURNAL OF CLINICAL HYPERTENSION, Issue 7 2007Javier Díez MD Changes in the composition of cardiac tissue develop in hypertensive patients with left ventricular hypertrophy (ie, hypertensive heart disease) and lead to structural remodeling of the myocardium. One of these changes is related to the disruption of the equilibrium between the synthesis and degradation of collagen types I and III molecules, which results in an excessive accumulation of collagen types I and III fibers within the myocardium. Myocardial fibrosis is the consequence of a number of pathologic processes mediated by mechanical, neurohormonal, and cytokine routes. The clinical relevance of fibrosis is that it may contribute to heart failure and other cardiac complications in patients with hypertensive heart disease. This brief review focuses on the mechanisms of hypertensive myocardial fibrosis. [source] Salutary effects of Corydalis yanhusuo extract on cardiac hypertrophy due to pressure overload in ratsJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 8 2007Chengping Wen We have evaluated the effects of an alcohol extract from the rhizome of Corydalis yanhusuo W.T. (CY), a well-known traditional Chinese medicinal herb, on pressure-overloaded cardiac hypertrophy induced by transverse abdominal aorta constriction (TAAC) in rats. Rats were given vehicle or CY extract (200 or 50 mg kg,1 per day) from the second week after induction of pressure overload, for a period of 7 weeks. Haemodynamic parameters, relative heart weight and myocyte cross-sectional area were measured in each group. We also estimated left ventricular (LV) collagen volume fraction (CVF) using Masson trichrome staining, and type I collagen expression by Western blot assay. Chronic TAAC caused notable cardiac hypertrophy and heart dysfunction. Significant collagen deposition and greater type I collagen expression were found in model control rats. These changes were not significantly reversed after treatment with 50 mgkg,1 CY, whereas 200 mgkg,1 significantly improved heart function and prevented cardiac hypertrophy, with parallel reductions in myocardial fibrosis, as evidenced by reduced LV CVF and reduced levels of type I collagen. In conclusion, chronic treatment of rats with CY extract attenuated development of cardiac hypertrophy. [source] Intramyocardial arterial narrowing in dogs with subaortic stenosisJOURNAL OF SMALL ANIMAL PRACTICE, Issue 9 2004T. Falk Earlier studies have described intramyocardial arterial narrowing based on hyperplasia and hypertrophy of the vessel wall in dogs with subaortic stenosis (SAS). In theory, such changes might increase the risk of sudden death, as they seem to do in heart disease in other species. This retrospective pathological study describes and quantifies intramyocardial arterial narrowing in 44 dogs with naturally occurring SAS and in eight control dogs. The majority of the dogs with SAS died suddenly (n=27); nine had died or been euthanased with signs of heart failure and eight were euthanased without clinical signs. Dogs with SAS had significantly narrower intramyocardial arteries (P<0.001) and more myocardial fibrosis (P<0.001) than control dogs. Male dogs and those with more severe hypertrophy had more vessel narrowing (P=0.02 and P=0.02, respectively), whereas dogs with dilated hearts had slightly less pronounced arterial thickening (P=0.01). Arterial narrowing was not related to age, but fibrosis increased with age (P=0.047). Dogs that died suddenly did not have a greater number of arterial changes than other dogs with SAS. This study suggests that most dogs with SAS have intramyocardial arterial narrowing and that the risk of dying suddenly is not significantly related to the overall degree of vessel obliteration. [source] Pulmonary oedema in Swedish hunting dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 5 2003A. Egenvall A syndrome of acute dyspnoea after hunting in 16 Swedish hunting dogs is characterised. Radiographic pulmonary infiltrates interpreted as pulmonary oedema were found in the acute stage. In 12 dogs, the infiltrates regressed after five to 14 days. Subendocardial necrosis and pulmonary oedema were found at postmortem examination in four other dogs with acute and recurrent dyspnoea after hunting, and myocardial fibrosis in a further three dogs with a history of recurrent dyspnoea after hunting; none of these pathological changes was seen in dogs which had no previous history of dyspnoea after hunting. A pathogenetic mechanism is proposed whereby high catecholamine levels, present during hunting due to the stress of excitement and exercise, cause acute cardiac and pulmonary lesions in some susceptible dogs, similar to neurogenic or postictal pulmonary oedema. [source] Characterization of the Electroanatomic Substrate for Monomorphic Ventricular Tachycardia in Patients with Nonischemic CardiomyopathyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2002HENRY H. HSIA HSIA, H.H., et al.: Characterization of the Electroanatomic Substrate for Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy. Ventricular arrhythmias are common in the setting of nonischemic cardiomyopathy. The etiology for the cardiomyopathy is frequently not identified and the label of "idiopathic" is applied. Interstitial fibrosis with conduction system involvement and associated left bundle branch block characterizes the disease process in some patients and the mechanism for monomorphic ventricular tachycardia is commonly bundle branch reentry. However, most patients with nonischemic cardiomyopathy have VT due to myocardial reentry and demonstrate marked myocardial fibrosis and electrogram abnormalities. Although patient specific, the overall distribution of electroanatomic abnormalities appears to be equal on the endocardium and epicardium. The extent of electrogram abnormalities appears to parallel arrhythmia presentation and/or inducibility. Patients with sustained uniform morphology VT have the most extensive endocardial and epicardial electrogram abnormalities. Magnetic electroanatomic voltage mapping provides a powerful tool to characterize the location and extent of the arrhythmia substrate. Basal left ventricular myocardial involvement, as indexed by the location of contiguous electrogram abnormalities, is common in patients with sustained VT and left ventricular cardiomyopathy. The relatively equal distribution of electrogram abnormalities on the endocardium and epicardium, and the results of mapping and ablation attempts, suggest that critical parts of the reentrant circuit may be epicardial. Unique features of the electroanatomic substrate associated with cardiomyopathy due to Chagas' disease, sarcoidosis, and arrhythmogenic right ventricular dysplasia are also discussed. [source] Transforming growth factor ,1 genotype and change in left ventricular mass during antihypertensive treatment,results from the swedish irbesartan left ventricular hypertrophy investigation versus atenolol (Silvhia)CLINICAL CARDIOLOGY, Issue 3 2004Pär Hallberg M.D. Abstract Background: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor ,1(TGF-,1); AT1-receptor antagonists reverse these changes. The TGF-(,1 G + 915C polymorphism is associated with in-terindividual variation in TGF- ,1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment. Hypothesis: We aimed to determine whether the TGF- ,1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1 -receptor antagonists or a beta1 -adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group. Methods: We determined the association between the TGF-,1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1 -receptor antagonist irbesartan or the beta1 -adrenoceptor blocker atenolol. Results: Irbesartan-treated patients who were carriers of the C-allele, which is associated with low expression of TGF-,1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI ,44.7 g/m2 vs. ,22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group. Conclusions: The TGF- ,1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1 -receptor antagonist irbesartan. [source] | ||||||||||