Fibrosis In Hypertensive Patients Research Articles

Left ventricle structure and function relations with the levels of plasma markers of fibrosis in hypertensive patients with NonSTEMI

Abstract Funding Acknowledgements Type of funding sources: None. Introduction. The myocardial fibrosis lies in the basis of left ventricle remodelling in patients with hypertension. Cardiomyocites hypertrophy, fibroblasts proliferation, enlargement of interstitial collagen volume and their ratio disorders may increase severity of stroke and myocardial infarction. Purpose. The purpose of the study is to evaluate relations between the plasma levels of myocardium fibrosis markers and left ventricle remodelling, systolic and diastolic function in hypertensive patients with NonSTEMI. Methods. Were examined 138 hypertensive patients (both men and women) with NonSTEMI. The mean age of patients was 51.2 (11.2) years. Patients with arrhythmias and conduction abnormalities, diabetes mellitus and autoimmune diseases were excluded form the study. In all patients was performed ECG in 12 standard leads; EchoCG (according to ASE/EACVI 2015 recommendations); evaluation plasma levels of tissue inhibitor of metalloproteinases-1 (TIMP-1) and insulin-like growth factor 1 (IGF-1). HF NYHA functional class was determined by performing 6MWT. Statistical significance was defined at the level of methods for p < 0,05. Results. The averaged levels for plasma markers of myocardium fibrosis were: TIMP-1 - 322.0 (250.0; 483.5) ng/mL; IGF-1 - 160.0 (141.0; 175.0) ng/mL. Results of correlative analysis revealed relations between IGF-1 and ILV mass (R=-0.59; p < 0.001), and weak correlation between IGF-1 and E/e" averaged (R=-0.19; p = 0.027) (Picture 1). These negative correlations may be explained by the growth in both fibroblasts and collagen production in myocardium. Also there were positive correlations between TIMP-1 and ILV mass (R = 0.63; p < 0.001) and TIMP-1 and E/e" average (R = 0.37; p < 0.001) (Picture 1) which may be due to an increase of myocardial stiffness as the result of fibrosis activity. The results of the comparison of TIMP-1 and ICF-1 plasma levels, structural and functional parameters of the LV in groups of patients with different types of LV geometry can be seen in Table 1. Conclusion. Thus, the results of the study show that plasma markers of fibrosis was significantly higher in patients with concentric and eccentric LV hypertrophy which may reflects the higher levels of myocardium stiffness. Abstract Table 1. Abstract Figure. Picture 1.

72. MYOCARDIAL FIBROSIS IN HYPERTENSIVE PATIENTS: A NOVEL TARGET IMAGING BIOMARKER

Background: Myocardial fibrosis is essential in pathological basis of many cardiovascular diseases. Cardiac magnetic resonance (CMR) using T1 mapping serves to identify interstitial fibrosis in many cases, one of which is hypertension. It is suggested that T1 mapping in hypertensive patients compared to other cardiovascular risk factors share similar values that is strongly linked to cardiovascular morbidity including increased ischemic burden, decreased systolic function, and cardiovascular death. Objective: To identify the extend of myocardial fibrosis in hypertensive patients compared to other cardiovascular risk factors. Methods: The study was conducted in Department of Cardiology and Vascular Medicine Universitas Indonesia/National Cardiovascular Center Harapan Kita. Analysis was performed on data extracted from cardiac magnetic resonance examinations on all hypertensive patients consulted to the imaging division in January-December 2018. A total of 120 subjects underwent scanning on a 1.5-Tesla Philips Achieva scanner. At rest, mid LV native T1 map was acquired using the Look-Locker methods. Results: Overall, the majority of participants were male (73%) with mean age of 57.22 ± 10.01 years and mean body mass index of 25.75 ± 4.40. The number of subjects with diabetes mellitus, dyslipidemia, and smokers were 40%, 50%, and 22% respectively. There is no difference between T1 value of patients who were hypertensive with no other cardiovascular risk factors (n = 19, mean T1 1253.63 ± 347.48) and hypertensive patients carrying other risk factors (n = 34, mean T1 1250.66 ± 365.42), p = 0.75. In addition, both groups showed no difference in terms of left ventricular systolic function with mean ejection fraction (EF) of 48.6% in those with hypertension alone and EF of 45.4% in hypertensive patients with other additional risk factors (p = 0.48). Conclusion: Hypertension alone had similar extent of myocardial fibrosis to those with any other additional cardiovascular risk factors. Since extent of myocardial fibrosis is strongly linked to cardiovascular death, this finding should be brought into more careful investigation in the future.

36. ASSOCIATION OF ELECTROCARDIOGRAM PARAMETERS OF ATRIAL AND VENTRICULAR REMODELING WITH INTERSTITIAL FIBROSIS IN HYPERTENSIVE PATIENTS

Background: Cardiac remodeling is frequently seen in hypertensive patients and one of the causes of its process is interstitial fibrosis. Electrocardiogram (ECG) is a practical tool to detect impulse heterogeneity, reflecting fibrosis. Objective: To prove association of ECG parameters with interstitial fibrosis in hypertension which might be used to monitor effectiveness of therapies and prognosis. Methods: This is a cross-sectional study whose subjects were diagnosed with hypertension recruited from public healthcare from December 2018 until January 2019. Exclusion criteria were elderly (>65 years old), known coronary artery disease, heart failure, and valvular heart diseases. Association between ECG parameters which reflects atrial remodeling, represented by P-wave Dispersion (PWD), and ventricular remodeling, represented by QT dispersion (QTd), with degree of interstitial fibrosis, represented by soluble ST2 (SST2) from blood serum, which has been proven for detecting myocardial fibrosis, were analyzed using Spearman's correlation. Multivariate analysis was performed to adjust the outcome with age and sex. Results: From 36 subjects recruited, 24 (66.7%) subjects were female. The median age was 57 (45-65) years old. There were significant moderate correlations between SST2 with PWD (p 0.001; r 0.498), and QTd (p 0.002; r 0.462). After multivariate analysis, the correlation remains significant for PWD (p 0.001) and QTd (p 0.018). The moderate correlation between ECG parameters and SST2 maybe due to the fibrosis caused by myocardial damage in hypertension is subtler than heart failure. Conclusion: There are moderate correlations between ECG parameters of atrial and ventricular remodeling with interstitial fibrosis in hypertensive patients.

AdipoRon Attenuates Hypertension-Induced Epithelial-Mesenchymal Transition and Renal Fibrosis via Promoting Epithelial Autophagy.

Hypertension-induced epithelial-mesenchymal transition (EMT) is a major mechanism of renal fibrosis. Adiponectin protects against hypertension-induced target organ damage. AdipoRon is an orally active synthetic adiponectin receptor agonist. However, it is unclear whether AdipoRon could attenuate EMT and renal fibrosis in hypertensive mice. C57BJ/6J mice were utilized to induce DOCA-salt-sensitive hypertensive model. Hypertension results in an altered adiponectin expression and promotes EMT in the kidney. In vitro, AdipoRon inhibits aldosterone (Aldo)-induced EMT and promotes autophagic flux in HK-2 epithelial cells. Mechanically, AdipoRon activates AMPK/ULK1 pathway in epithelial cells. Blockade of AMPK activation, as well as inhibition of autophagy, blocks the effects of AdipoRon on Aldo-induced EMT. Moreover, AdipoRon treatment promotes autophagy and improves renal fibrosis in DOCA-salt-hypertensive mice. Our data suggest that AdipoRon could be a potential therapeutic option to prevent renal fibrosis in hypertensive patients. Graphical abstract.

Comprehensive assessment of hypertensive heart disease: cardiac magnetic resonance in focus.

Arterial hypertension represents the most frequent cardiovascular risk factor that is associated with cardiac remodeling. Hypertensive heart disease was defined by the presence of left ventricular hypertrophy (LVH) and diastolic dysfunction, and it has been diagnosed by echocardiography in everyday clinical practice. Interstitial myocardial fibrosis is the underlying cause of hypertension-induced cardiac remodeling, and it could not be visualized with different echocardiographic methods. Cardiac magnetic resonance (CMR) and its methods such as late gadolinium enhancement, and T1 mapping provides qualitative and quantitative assessment of interstitial myocardial fibrosis in hypertensive patients. Furthermore, CMR canprovide differentiation of LVH between hypertensive patients and cardiomyopathies (hypertrophic or Fabry disease). Timely diagnosis of cardiac impairment and early treatment is essential because regression of LVH could be achieved with adequate treatment. Diffuse cardiac fibrosis in hypertensive patients might be an underlying mechanism that explains the increased cardiovascular morbidity and mortality in this population. Future longitudinal investigations are necessary to determine causal relationship between diffuse fibrosis and cardiovascular outcome in these patients. The aim of this review is to summarize the current knowledge regarding CMR techniques and their potential usage in patients with hypertensive heart disease.

CMR based measurement of aortic stiffness, epicardial fat, left ventricular myocardial strain and fibrosis in hypertensive patients

IntroductionA combined assessment of different parameters of cardiovascular (CV) risk and prognosis can be supportive and performed with cardiac magnetic resonance (CMR). Aortic stiffness, epicardial fat volume (EFV), left ventricular (LV) strain and fibrosis were evaluated within a single CMR examination and results were related to the presence of hypertension (HTN) and diabetes mellitus (DM). Methods20 healthy controls (57.2 ± 8.2 years(y); 26.2 ± 3.9 kg/m2), 31 hypertensive patients without DM (59.6 ± 6.7 y; 28.4 ± 4.7 kg/m2) and 12 hypertensive patients with DM (58.8 ± 9.9y; 30.7 ± 6.3 kg/m2) were examined at 1.5Tesla. Aortic stiffness was evaluated by calculation of aortic pulse wave velocity (PWV), EFV by a 3D-Dixon sequence. Longitudinal & circumferential systolic myocardial strain (LS; CS) were analyzed and T1-relaxation times (T1) were determined to detect myocardial fibrosis. ResultsEFV was highest in hypertensive patients with diabetes (78.4 ± 28.0 ml/m2) followed by only hypertensive patients (64.2 ± 27.3 ml/m2) and lowest in controls (50.3 ± 22.7 ml/m2; p < 0.05). PWV was higher in hypertensive patients with diabetes (9.8 ± 3.3 m/s) compared to only hypertensive patients (8.6 ± 1.7 m/s; p < 0.05) and to controls (8.1 ± 1.9 m/s; p < 0.05). LS&CS were worse in hypertensive patients with diabetes (LS:-20.9 ± 5.1% and CS: −24.4 ± 5.7%) compared to both only hypertensive patients (LS: −24.7 ± 4.6%; CS: −27.1 ± 5.0%; p < 0.05) and to controls (LS: −25.5 ± 3.8; CS: −28.3 ± 4.1%; p < 0.05). Both hypertensive groups with and without DM had higher T1́s (994.0 ± 43.2 ms; 991.6 ± 35.5 ms) than controls (964.6 ± 40.3 ms; p < 0.05). ConclusionCMR revealed increased aortic stiffness and EFV in hypertensive patients, which were even higher in the presence of DM. Also signs of LV myocardial fibrosis and a reduced strain were revealed. These parameters support the assessment of CV risk and prognosis. They can accurately be measured with CMR within a single examination when normally different techniques are needed.

P3838Evaluation of echocardiographic determinants of interatrial block in patients with essential hypertension

Abstract Introduction Interatrial block (IAB), defined as a conduction delay between the right and left atrium, is manifested on the electrocardiogram as a prolonged P-wave duration. Large number of studies recently have been published regarding the prevalence of IAB and its associations with cardiovascular events. It has been previously reported that myocardial fibrosis may cause conduction delays in hypertensive patients. In this study, we aimed to investigate the echocardiographic determinants of IAB in patients with hypertension. Methods This study enrolled a total of 220 patients [male: 93 (42.3%), mean age: 61.8±7.8 years] with hypertension. Patients with atrial fibrillation were excluded. IAB was defined as P wave duration of ≥120 ms with or without presence of notching. Routinely obtained 12-lead electrocardiography recordings were examined, and patients were divided into two groups as those with and without IAB. All patients were evaluated by transthoracic echocardiography. Results Electrocardiography revealed IAB in 70 patients. The baseline demographic characteristics of the patients with and without IAB were similar in both groups. Left atrial diameter (LAD), interventricular septal thickness, posterior wall thickness, left ventricular mass, left ventricular mass index, and the prevalence of left ventricular hypertrophy (LVH) were found to be significantly increased in hypertensive patients with IAB. Increased LAD (OR=1.082; 95% CI: 1.006–1.164; p=0.034) and LVH (OR=3.051; 95% CI: 1.164–7.994; p=0.023) were found to be independent predictors of IAB. In the receiver operating characteristic curve analyses, LAD values above 38 mm predicted IAB with a sensitivity of 68%, and a specificity of 58% (AUC= 0.678; 95% CI: 0.601–0.754; p&lt;0.001). Conclusion A significant association exists between the presence of IAB and echocardiographic parameters related to left ventricular hypertrophy and left atrial dilatation in patients with essential hypertension. The presence of IAB may be used as an electrocardiographic marker of cardiac remodelling and myocardial fibrosis in hypertensive patients.

Fragmented QRS as a Marker of Myocardial Fibrosis in Hypertension: a Systematic Review.

Hypertension cause damage in cardiac structure and induce pathological myocardial fibrosis that leads to hypertensive cardiomyopathy. A narrow fragmented QRS complex (fQRS) is associated with myocardial fibrosis and scar tissue in various cardiovascular diseases. It is also associated with myocardial fibrosis in hypertensive patients even in the absence of any structural heart diseases. This article aimed to demonstrate importance and usefulness of fQRS in hypertensive patients. Current evidence suggest that the frequency of fQRS is significantly higher in hypertensive patients compared to normotensives. Also, fQRS seems to be a predictor of left ventricular hypertrophy, increased systolic blood pressure, non-dipping, deterioration of the left ventricular geometry, and worse systolic and diastolic functions in hypertensive patients. As a simple and easy detectable electrocardiographic finding, fQRS may indicate myocardial fibrosis, uncontrolled blood pressure, and deteriorated cardiac structure in hypertensive patients even in the absence of other structural heart diseases, and may also be useful to predict high-risk hypertensives.

The Relationship between the Retinal Nerve Fiber Layer Thickness and the Presence of Fragmented QRS Complexes in Patients with Hypertension

Background: Fragmented QRS (fQRS) detected on electrocardiography (ECG) has been demonstrated to be a marker of myocardial fibrosis in hypertensive patients. Retinal microvascular abnormalities reflect cumulative microcirculatory damage resulting from hypertension and atherosclerosis. In this study, we aimed to evaluate the retinal nerve fiber layer (RNFL) thickness in hypertensive patients with and without fQRS complexes detected on ECG. Methods: Consecutive patients who were diagnosed with hypertension were included in the study. ECG and transthoracic echocardiography were performed to all patients. fQRS was defined as additional R’ wave or notching/splitting of S wave in two contiguous ECG leads. The RNFL thickness was measured by a spectral-domain optical coherence tomography device along a circle around the center of the optic disc. Results: This observational case-control study enrolled 62 (42 female, mean age: 54.3±9.9 years) hypertensive patients with fQRS and 42 (24 female, mean age: 53.1±11.8 years) hypertensive control patients without fQRS between April 2017 and October 2017. There was no significant difference between groups regarding demagraphic, laboratory and echocardiographic parameters. In all retinal quadrants, the mean RNFL thickness did not differ significantly between patients with fQRS(+) and fQRS(-) group. Conclusion: The presence of fQRS in the ECG had no significant effect on the RNFL thickness in hypertensive patients. Detection of fQRS may not be used as a useful non-invasive technique in the evaluation of atherosclerosis in hypertensive patients.

P6575Relations between left ventricle remodelling, renin-angiotensin-aldosteron system activity and plasma markers of fibrosis in hypertensive patients with CAD underwent PCI

P6575Relations between left ventricle remodelling, renin-angiotensin-aldosteron system activity and plasma markers of fibrosis in hypertensive patients with CAD underwent PCI

Phenotyping of myocardial fibrosis in hypertensive patients with heart failure. Influence on clinical outcome.

Myocardial fibrosis is associated with alterations in the cross-linking and deposition of collagen type I (CCL and CD, respectively). We aimed to evaluate whether the combination of circulating biomarkers of CCL [the carboxy-terminal telopeptide of collagen type I to matrix metalloproteinase-1 ratio (CITP : MMP-1)] and CD [the carboxy-terminal propeptide of procollagen type I (PICP)] identifies myocardial fibrosis phenotypes with distinct clinical outcome in hypertensive patients with heart failure. Endomyocardial biopsies and blood samples from 38 patients (small cohort), and blood samples from 203 patients (large cohort) were analyzed. Myocardial CCL and CD were assessed by histological methods. Serum PICP, CITP, and MMP-1 were determined by ELISA. Small cohort: CITP : MMP-1 cutoff 1.968 or less and PICP cutoff at least 110.8 ng/ml were used for predicting high CCL and severe CD, respectively. Large cohort: as defined by the above thresholds, patients were categorized into four subgroups based on the presence (+) or absence (-) of high CCL and severe CD. Compared with CCL-CD-, the adjusted hazard ratios for a composite end point of heart failure hospitalization or cardiovascular death over 5 years in CCL-CD+, CCL+CD-, and CCL+CD+ were 1.11 (P = 0.79), 1.99 (P = 0.07), and 2.18 (P = 0.04), respectively (P for trend = 0.005). In addition, the categorization based on CCL and CD yielded integrated discrimination (P = 0.03) and net reclassification (P = 0.01) improvements for the mentioned outcome. The combination of low serum CITP : MMP-1 ratio and high serum PICP identifies hypertensive patients with heart failure presenting with a phenotype of myocardial fibrosis characterized by the concurrence of excessive CCL and CD and associated with poor outcome.

Procollagen type III amino terminal peptide and myocardial fibrosis: A study in hypertensive patients with and without left ventricular hypertrophy

Introduction and ObjectivesAn exaggerated accumulation of type I and type III fibrillar collagens occurs throughout the free wall and interventricular septum of patients with primary hypertension and left ventricular hypertrophy (LVH). In the present study the serum concentration of procollagen type III amino terminal peptide (PIIIP) was measured to determine the value of this peptide as a potential marker of ventricular fibrosis in hypertensive patients, particularly those with LVH. MethodsThe study population consisted of patients with never-treated mild to moderate essential hypertension and 30 normotensive control subjects. Clinical, echocardiographic, electrocardiographic and biochemical parameters were assessed in all patients. ResultsHeart rate, body mass index and levels of blood pressure were increased in hypertensives, particularly those with LVH, compared to normotensive controls. Posterior wall thickness, left ventricular (LV) mass and LV mass index, and serum PIIIP concentration were also increased in hypertensives, with significant differences between the two hypertensive groups. The ratio between maximal early and late transmitral flow velocity measured during diastole was lower in hypertensives, particularly those with LVH, than in normotensive controls. ConclusionsThe increase in PIIIP indicates that type III collagen synthesis increases in hypertensives, particularly those with LVH, implying that alterations in the heart in hypertension are the result not solely of hypertrophied LV muscle, but also of increased collagen deposition within the ventricular wall and around the coronary vessels.Thus, measurement of serum PIIIP could be a practical and useful tool in the non-invasive assessment of myocardial remodeling in hypertension.

Procollagen type III amino terminal peptide and myocardial fibrosis: A study in hypertensive patients with and without left ventricular hypertrophy

Introduction and ObjectivesAn exaggerated accumulation of type I and type III fibrillar collagens occurs throughout the free wall and interventricular septum of patients with primary hypertension and left ventricular hypertrophy (LVH). In the present study the serum concentration of procollagen type III amino terminal peptide (PIIIP) was measured to determine the value of this peptide as a potential marker of ventricular fibrosis in hypertensive patients, particularly those with LVH. MethodsThe study population consisted of patients with never-treated mild to moderate essential hypertension and 30 normotensive control subjects. Clinical, echocardiographic, electrocardiographic and biochemical parameters were assessed in all patients. ResultsHeart rate, body mass index and levels of blood pressure were increased in hypertensives, particularly those with LVH, compared to normotensive controls. Posterior wall thickness, left ventricular (LV) mass and LV mass index, and serum PIIIP concentration were also increased in hypertensives, with significant differences between the two hypertensive groups. The ratio between maximal early and late transmitral flow velocity measured during diastole was lower in hypertensives, particularly those with LVH, than in normotensive controls. ConclusionsThe increase in PIIIP indicates that type III collagen synthesis increases in hypertensives, particularly those with LVH, implying that alterations in the heart in hypertension are the result not solely of hypertrophied LV muscle, but also of increased collagen deposition within the ventricular wall and around the coronary vessels.Thus, measurement of serum PIIIP could be a practical and useful tool in the non-invasive assessment of myocardial remodeling in hypertension.

Association of fragmented QRS complexes on ECG with left ventricular diastolic function in hypertensive patients.

Diastolic dysfunction occurs as a result of interstitial fibrosis in hypertensive patients. Fragmented QRS (fQRS) on ECG signifies myocardial fibrosis in various clinical situations. We investigated whether fQRS on ECG is related to diastolic dysfunction in patients with hypertension. The study population included 72 hypertensive patients with normal coronary angiogram. Fragmented QRS was defined as the presence of an additional R wave (R'), notching of the R or S wave or fragmentation in two contiguous leads corresponding to a major coronary artery. Echocardiography was performed to all patients to detect diastolic dysfunction. Diastolic dysfunction was regarded as non-severe if patients had normal diastolic function or grade 1 diastolic dysfunction or severe if they had grade ≥2 diastolic dysfunction. Thirty-two patients had fQRS on ECGs (fQRS [+] group) and there were 40 patients who did not have fQRS on their ECGs (fQRS [-] group). The two groups were similar in terms of baseline characteristics. In patients with fQRS on the ECG, severe diastolic dysfunction was more prevalent (59.4% vs. 7.5%, p<0.001). The duration of hypertension was longer in patients with fQRS on the ECG (p<0.001). The presence of fQRS on the ECG was an indicator for severe diastolic dysfunction (B=1.954; odds ratio=7; 95% confidence interval=1.4-35.4; p=0.018). The presence of fQRS complexes on ECG predicts more severe diastolic dysfunction in patients with hypertension.

Increased extracellular volume and altered mechanics are associated with left ventricular hypertrophy in hypertensive heart disease, not hypertension alone

Background Study purpose To detect differences in extracellular volume (ECV) and systolic strain in hypertensive patients with LVH as compared to hypertensive patients without LVH and age-matched controls. Background: Increased ECV due to diffuse myocardial fibrosis in hypertensive patients may be an underlying mechanism contributing to increased cardiovascular risk. Moreover HTN patients with left ventricular hypertrophy (LVH) are at higher risk of cardiovascular morbidity and mortality when compared to HTN Non-LVH subjects. We compared levels of ECV and systolic strain between HTN LVH, HTN Non-LVH and control subjects.

Association of Cardiotrophin-1 With Myocardial Fibrosis in Hypertensive Patients With Heart Failure

Cardiotrophin-1 has been shown to be profibrogenic in experimental models. The aim of this study was to analyze whether cardiotrophin-1 is associated with left ventricular end-diastolic stress and myocardial fibrosis in hypertensive patients with heart failure. Endomyocardial biopsies from patients (n=31) and necropsies from 7 control subjects were studied. Myocardial cardiotrophin-1 protein and mRNA and the fraction of myocardial volume occupied by collagen were increased in patients compared with controls (P<0.001). Cardiotrophin-1 overexpression in patients was localized in cardiomyocytes. Cardiotrophin-1 protein was correlated with collagen type I and III mRNAs (r=0.653, P<0.001; r=0.541, P<0.01) and proteins (r=0.588, P<0.001; r=0.556, P<0.005) in all subjects and with left ventricular end-diastolic wall stress (r=0.450; P<0.05) in patients. Plasma cardiotrophin-1 and N-terminal pro-brain natriuretic peptide and serum biomarkers of myocardial fibrosis (carboxy-terminal propeptide of procollagen type I and amino-terminal propeptide of procollagen type III) were increased (P<0.001) in patients compared with controls. Plasma cardiotrophin-1 was correlated with N-terminal pro-brain natriuretic peptide (r=0.386; P<0.005), carboxy-terminal propeptide of procollagen type I (r=0.550; P<0.001), and amino-terminal propeptide of procollagen type III (r=0.267; P<0.05) in all subjects. In vitro, cardiotrophin-1 stimulated the differentiation of human cardiac fibroblast to myofibroblasts (P<0.05) and the expression of procollagen type I (P<0.05) and III (P<0.01) mRNAs. These findings show that an excess of cardiotrophin-1 is associated with increased collagen in the myocardium of hypertensive patients with heart failure. It is proposed that exaggerated cardiomyocyte production of cardiotrophin-1 in response to increased left ventricular end-diastolic stress may contribute to fibrosis through stimulation of fibroblasts in heart failure of hypertensive origin.

Blood pressure levels are the sole determinant of diffuse myocardial fibrosis in hypertensive patients

Blood pressure levels are the sole determinant of diffuse myocardial fibrosis in hypertensive patients

Influence of serum adiponectin level and SNP +45 polymorphism of adiponectin gene on myocardial fibrosis

Adiponectin plays an important role in the development of hypertension, atherosclerosis, and cardiomyocyte hypertrophy, but very little was known about the influence of serum adiponectin or the adiponectin gene polymorphism on myocardial fibrosis. Our study investigates the influence of the SNP +45 polymorphism of the adiponectin gene and serum levels of adiponectin on myocardial fibrosis in patients with essential hypertension. A case-control study was conducted on 165 hypertensive patients and 126 normotensive healthy controls. The genotypes of adiponectin gene polymorphisms were detected by the polymerase chain reaction (PCR) method. Serum concentrations of procollagen were measured by a double antibody sandwich enzyme-linked immunosorbent assay (ELISA) in all subjects. The integrated backscatter score (IBS) was measured in the left ventricular myocardium using echocardiography. The serum levels of adiponectin in hypertensive patients were significantly lower than those in the normal control group ((2.69±1.0) μg/ml vs. (4.21±2.89) μg/ml, respectively, P<0.001). The serum levels of type-I procollagen carboxyl end peptide (PICP) and type-III procollagen ammonia cardinal extremity peptide (PIIINP) in the hypertension group were significantly higher than those in the control group. In the hypertension group, serum levels of adiponectin were significantly and negatively related to the average acoustic intensity and corrected acoustic intensity of the myocardium (r=0.46 and 0.61, respectively, P<0.05 for both). The serum levels of PICP and PIIINP were significantly different among the three genotypes of SNP +45 (P<0.01). Logistic regression analyses showed that sex and genotype (GG+GT) were the major risk factors of myocardial fibrosis in hypertensive patients (OR=5.343 and 3.278, respectively, P<0.05). These data suggest that lower levels of adiponectin and SNP +45 polymorphism of the adiponectin gene are likely to play an important role in myocardial fibrosis in hypertensive patients.

Aortic stiffness is increased in acromegaly regardless the method of assessment

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Effects of Prolonged-Release Torasemide Versus Furosemide on Myocardial Fibrosis in Hypertensive Patients with Chronic Heart Failure: A Randomized, Blinded–End Point, Active-Controlled Study

Background The pharmacologic modification of the synthesis and deposition of fibrillar collagen in the myocardium may have effects on the cardiac function, clinical status, and prognosis of patients with heart failure (HF). Serum procollagen type I carboxyterminal peptide (PICP) is a biochemical marker of collagen type I fibers synthesis and myocardial deposition. Objective The aim of this study was to evaluate the effects of both the prolonged-release (PR) formulation of torasemide (torasemide-PR) and furosemide on myocardial fibrosis in hypertensive patients with chronic HF. Methods This was a multicenter, parallel-group, randomized, open-label study with blinded evaluation of data (PROBE: Prospective Randomized Open-label Blinded End points). Patients were randomly assigned to treatment with torasemide-PR (n = 77) or furosemide (n = 78), while receiving the best standard chronic HF treatment. Effects of torasemide-PR and furosemide on myocardial fibrosis were assessed through PICP serum levels. Twenty-eight patients discontinued prematurely from the study, 14 in each treatment group. Results One hundred fifty-five patients were randomized, 58.1% of whom were male. Mean (SD) age of the patients was 68.1 (11.4) years in the torasemide-PR group and 69.3 (9.8) years in the furosemide group. At baseline, 96.1% of patients in the torasemide-PR group and 89.7% in the furosemide group had NYHA class II HF. Most patients in both treatment groups presented with preserved ejection fraction (EF >40%). No differences were found in PICP serum levels at the end of the study between patients treated with torasemide-PR and patients treated with furosemide ( P = 0.75). Adjusted difference (95% CI) for baseline concentration between both treatment groups was −1.2 (−8.9 to 6.4). Conclusions In hypertensive patients with mild and clinically stable HF, long-term administration of either torasemide-PR or furosemide was not associated with significant effects on myocardial fibrosis, as assessed by serum PICP. ClinicalTrials.gov identifier: NCT00409942.