358 research outputs found

    Myocardial fibrosis in isolated left ventricular non-compaction and its relation to disease severity

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    Aims The aim of the present study was to evaluate the prevalence and extent of myocardial fibrosis in patients with isolated left ventricular non-compaction (LVNC) and to determine its relation to clinical status and LV systolic function. Methods and results The cardiac magnetic resonance imaging (MRI) database of our institution was searched for all patients with a first diagnosis of isolated LVNC. The diagnosis of isolated LVNC was based on the presence of standard cardiac MRI and clinical criteria. For each patient, cine and contrast-enhanced cardiac MR images were analysed to evaluate LV systolic function and the prevalence and extent of late gadolinium enhancement (LGE), a surrogate of myocardial fibrosis. A total of 42 patients (mean age 46 ± 20 years, 62% male) were identified. Late gadolinium enhancement was observed in 23 (55%) patients with isolated LVNC, occupying 4.8 ± 6.7% of the LV mass. Both the presence and extent of LGE were significantly related to the number of abnormal clinical features (i.e. symptomatic status, resting electrocardiogram abnormalities, and 24 h Holter monitoring abnormalities; P <, 0.001 and P = 0.001, respectively). Similarly, LGE was more prevalent and extensive in patients with LV ejection fraction (EF),<50% compared with patients with LVEF ≥50% (90 vs. 23%; P <, 0.001 and 8.9 ± 7.6 vs. 1.1 ± 2.4%; P <, 0.001, respectively). At multivariate analysis, both the presence and extent of LV LGE were independently related to LVEF (β = -0.63; P <, 0.001 and β = -0.62; P <, 0.001, respectively). Conclusion Myocardial fibrosis is related to clinical disease severity and LV systolic dysfunction in isolated LVNC. © 2010 The Author

    Relationship between triiodothyronine and proinflammatory cytokines in chronic heart failure

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    Cytokines and thyroid hormones are involved in the biochemical changes associated to heart failure (HF). AIM: Aims of the study were to investigate: plasma circulating levels of the cytokines Interleukine-6 (IL-6) TNF alpha and C reactive protein (CRP) in patients with stable HF in relation to the severity of left ventricular dysfunction; the relationship between these inflammatory markers and thyroid hormones. METHODS: One-hundred and sixty-six patients (121 males, age 64+/-12), with non-ischemic cardiomyopathy, were admitted to the Institute of Clinical Physiology for progressive deterioration of symptoms. Forty-eight healthy subjects (30 males, age range 26-75 years) were also enrolled as control group (Group N). High sensitivity (hs)-IL-6 and hs-TNFalpha were quantified using solid phase sandwich ELISA kits. Hs-CRP was measured by Immulite System. RESULTS: In the whole population (HF and N), the association between inflammatory markers and age resulted statistically significant only for IL-6 serum concentration (p35% and EF<35%, we clearly observed the progressive enhancement of the inflammatory markers. Considering normal subjects, patients without and with low T3 syndrome, IL-6 and TNFalpha increased progressively from normal to patients with fT3<2 pg/ml (p<0.01 and p<0.01) while CRP only respect to the group with low T3 syndrome (p<0.01). The inflammatory markers were all inversely correlated with FT3 levels. CONCLUSION: Because low FT3 serum concentration represents a negative prognostic index, it is likely that impairment of T3 production and enhanced inflammation represent pathogenic mechanisms linked to HF progression

    Myocardial blood flow and fibrosis in hypertrophic cardiomyopathy

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    Abstract BACKGROUND: We investigated the relationship between myocardial blood flow (MBF), fibrosis, risk factors for sudden death, and clinical manifestations in hypertrophic cardiomyopathy (HCM). METHODS AND RESULTS: Sixty-two patients with HCM (45 men, overall mean age 47 ± 16 years), 15 acromegalic patients with left ventricular hypertrophy (9 man, overall mean age 47 ± 12 years), and 20 healthy subjects underwent cardiac magnetic resonance. Resting MBF was measured as the ratio between coronary sinus flow measured by phase-contrast technique and left ventricular mass. Myocardial fibrosis was evaluated by late gadolinium enhancement (LGE) technique. In HCM patients, MBF was significantly lower than in control subjects and acromegalic patients. Patients with LGE had lower MBF than those without it (0.46 ± 0.2 vs 0.66 ± 0.29 mL·min(-1)·g(-1); P < .005). Patients with ventricular tachycardia at Holter monitoring had lower MBF (0.4 ± 0.14 vs 0.6 ± 0.29 mL·min(-1)·g(-1); P < .04). Among patients with preserved systolic function, those in New York Heart Association (NYHA) functional class ≥II had lower MBF than those in NYHA functional class I (0.46 ± 0.2 vs 0.69 ± 0.3 mL·min(-1)·g(-1); P < .003). MBF was the only independent predictor of worse clinical status (NYHA ≥II; P = .01). CONCLUSIONS: In HCM patients low resting MBF is associated with the presence of fibrosis. MBF is a predictor of worse clinical status
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