Biomarkers of Myocardial Stress and Fibrosis as Predictors of Mode of Death in Patients With Chronic Heart Failure
Tariq AhmadMona FiuzatBenjamin A. NeelyMegan L. NeelyMichael PencinaWilliam E. KrausFaı̈ez ZannadDavid J. WhellanMark DonahueIleana L. PiñaKirkwood F. AdamsDalane W. KitzmanChristopher M. O’ConnorG. Michael Felker
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Myocardial fibrosis
Chronic Stress
The purpose of this study was to assess the effects of 12 weeks of atorvastatin treatment on myocardial fibrosis in patients with hypertension with atherosclerosis. 15 statin-naïve participants (11 males; mean age 67±10 years) with atherosclerosis were given atorvastatin (40 mg/day) for 12 weeks and underwent echocardiography including ultrasonic tissue characterization by cyclic variation of integrated backscatter (CVIBS). Serum galectin-3 and fibrosis markers including aminoterminal propeptide of type III procollagen (PIIINP), matrix metalloproteinase-2, metalloproteinase-9, and tissue inhibitor of metalloproteinase-1 (TIMP-1) were also analyzed. After 12 weeks of atorvastatin (40 mg/day) treatment, serum total cholesterol and low-density lipoprotein cholesterol decreased significantly (204±31 to 140±24 mg/dL and 133±26 to 69±17 ng/mL, respectively, both p<0.001). In myocardial fibrosis analysis, CVIBS increased significantly (6.6±1.9 to 8.5±2.7 dB, p=0.024). In addition, the circulating fibrosis markers serum PIIINP and TIMP-1 decreased significantly (9.5±2.7 to 6.4±1.4 ng/mL, p=0.012 and 299±65 to 250±45 ng/mL, p=0.024, respectively). 12 weeks of medium dose atorvastatin treatment resulted in a significant reduction in myocardial fibrosis as evaluated by morphofunctional parameters and plasma markers of tissue fibrosis.NTC00172419; results.
Myocardial fibrosis
Procollagen peptidase
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Myocardial fibrosis is caused by the excessive accumulation of collagen. It can be found in all stages of viral myocarditis,especially in the recovery and chronic stage. The myocardial fibrosis is regulated by many factors including direct viral tissue damage and indirect damage caused by transforming growth factor β1(TGF-β1),renin-angiotensin-aldosterone system, nitric oxide/endothelin,and mammalian target of rapamycin(mTOR). There is a lack of specificity in the clinical manifestations of myocardial fibrosis. The anti-fibrosis therapy is necessary only in the chronic stage of viral myocarditis.
Viral Myocarditis
Myocardial fibrosis
Cardiac Fibrosis
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Objective: To investigate the effects of ligustrazine (Li) on myocardial fibrosis in rats with pressure overload. Methods: Pressure overload rat models were established by constricting the abdominal aorta. Sixty-three SD rats were divided into 3 groups: Sham operated group (SOG, n=21), operated group (OG, n=21) and operated combined with ligustrazine group (OG+Li, n=21). Each group was randomly assigned to seven time points: The 1st, 2nd, 4th, 7th, 14th, 21st and 30th day after operation. Three rats were included in each time point. Serial sections of cardiac tissues were examined and the morphological or morphometric analysis of the SOG, OG and OG+Li done by histopathological and computer image analyzer technique. Results: (1) It showed that there were reactive fibrosis (from the 4th day on after operation) and reparative fibrosis (from the 21st day on after operation) in the OG, while myocardial fibrosis in the OG+Li was alleviated. Though reactive fibrosis (from the 21st day on after operation) was shown, reparative fibrosis wasn′t seen. (2) Perivascular collagen area (PVCA) in the OG (2. 09±0. 45) was significantly higher than SOG (0.83±0.06) from the 1st day on after operation and then steadily increased, while in the OG+Li (1. 16±0.06), it was significantly lower than OG at the same time; collagen volume fraction (CVF) in the OG (3. 08±0.56) significantly increased compared with the SOG (2. 78±0.64) from the 2nd day on after operation and showed a trend of rapid ascending from the 21st day on after operation; and in the OG+Li (4. 69±0.85), it was significantly decreased compared with the OG (7. 56±0.88) from the 21st day on after operation, with all P＜0. 05. Conclusion: Ligustrazine could alleviate and postpone the accumulation of myocardial collagen and has protective effects on the heart.
Pressure overload
Myocardial fibrosis
Cardiac Fibrosis
Abdominal aorta
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The hearts of 28 necropsy cases with DCM and 10 control cases were analysed to elucidate the role of myocarditis and fibrosis in dilated cardiomyopathy (DCM). The extent of fibrosis and myocyte diameter were measured in the transverse sections of the left ventricle. The degree and pattern of fibrosis varied widely from case to case. The DCM cases were then classified into 3 groups: 1) Group la, 8 cases with mild diffuse fibrosis; 2) Group Ib, 9 cases with severe diffuse fibrosis and 3) Group II, 11 cases with segmental fibrosis.Myocardial fibrosis and hypertrophy were significantly more prominent in Groups Ib and II than in the control group (p<0.01), but no differences were observed between Group la and the control group. Thus, it is reasonable to attribute the chronic CHF and LV dilatation in Groups Ib and II to the extensive myocardial fibrosis. In contrast, it is not reasonable to attribute the chronic CHF and LV dilatation in Group la to myocardial fibrosis.Focal lymphoid cell infiltration was graded to assess inflammatory changes. Group II showed more prominent inflammatory changes than the other 2 groups (p<0.05). Thus, it is possible that myocarditis is an etiologic factor for DCM with a segmental pattern of fibrosis.
Myocardial fibrosis
Dilated Cardiomyopathy
Endomyocardial fibrosis
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Myocardial fibrosis is the hallmark of myocardial remodelling found in hypertensive individuals. This process adversely affects the outcomes of such patients and results in diastolic and systolic cardiac dysfunction, electrical dysrhythmia and potentially sudden death. Collagen metabolism has been highlighted as the primary mechanism by which fibrosis is regulated. However, there are many other facets to the pathophysiology of myocardial fibrosis including mechanical, cellular and hormonal influences, which may guide therapy and thereby determine prognosis.
Myocardial fibrosis
Pathophysiology
Cardiac Fibrosis
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Left ventricular myocardial fibrosis in patients with aortic stenosis (AS) confers worse prognosis. Plasma osteoprotegerin (OPG), a cytokine from the TNF receptor family, correlates with the degree of valve calcification in AS, reflecting the activity of the tissue RANKL/RANK/OPG (receptor activator of nuclear factor κΒ ligand/RANK/osteoprotegerin) axis, and is associated with poorer outcomes in AS. Its association with myocardial fibrosis is unknown. We hypothesised that OPG levels would reflect the extent of myocardial fibrosis in AS. We included 110 consecutive patients with AS who had undergone late-gadolinium contrast enhanced cardiovascular magnetic resonance (LGE-CMR). Patients were characterised according to pattern of fibrosis (no fibrosis, midwall fibrosis, or chronic myocardial infarction fibrosis). Serum OPG was measured with ELISA and compared between groups defined by valve stenosis severity. Some 36 patients had no fibrosis, 38 had midwall fibrosis, and 36 had chronic infarction. Patients with midwall fibrosis did not have higher levels of OPG compared to those without fibrosis (6.78 vs. 5.25 pmol/L, p = 0.12). There was no difference between those with midwall or chronic myocardial infarction fibrosis (6.78 vs. 6.97 pmol/L, p = 0.27). However, OPG levels in patients with chronic myocardial infarction fibrosis were significantly higher than those without fibrosis (p = 0.005).
Myocardial fibrosis
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Myocardial fibrosis
Cardiac Fibrosis
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Abstract Myocardial fibrosis is observed in many cardiovascular diseases including hypertension, heart failure and cardiomyopathy. Myocardial fibrosis has been proved to be reversible and treatable only under timely intervention, which makes early detection and assessment of fibrosis crucial. Aside from tissue biopsy as the gold standard for the diagnosis of myocardial fibrosis, circulating biomarkers have been adopted as noninvasive assessment of this lesion. Dysregulated collagen deposition is thought to be the major cause of myocardial fibrosis. Collagens, procollagens, TGF-β, TIMP, galectin-3, and microRNAs are thought to be indicators of myocardial fibrosis. In this review, we summarize the molecules that are frequently used as biomarkers in diagnosis of cardiac fibrosis. Mechanisms of fibrosis that they take part in are also introduced.
Myocardial fibrosis
Cardiac Fibrosis
Gold standard (test)
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Although hypertensive heart disease (HHD) is clinically characterized by development of left ventricular hypertrophy in the absence of a cause other than arterial hypertension, changes in the composition of myocardial tissue also develop in arterial hypertension, leading to structural remodeling of the myocardium (eg, fibrosis). Myocardial fibrosis is the major determinant of diastolic dysfunction/failure in patients with HHD. Recent available data on the determination of serum concentrations of collagen-derived serum peptides, as well as quantitative analysis of echoreflectivity to address the presence of fibrosis in the myocardium of hypertensive patients, are promising. In addition, preliminary data suggest that the goal of reducing myocardial fibrosis is achievable using specific pharmacological agents in patients with HHD. (Circ J 2008; Suppl A: A-8 - A-12)
Hypertensive heart disease
Myocardial fibrosis
Myocardial hypertrophy
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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.
Hypertensive heart disease
Myocardial fibrosis
Cardiac Fibrosis
Clinical Significance
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