PubMed · 9277972
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M Yamakado. 1997. [Heart failure].. https://pubmed.ncbi.nlm.nih.gov/9277972/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are considered to be the most specific and sensitive biochemical markers of myocardial damage. Troponins have been studied in a wide range of clinical settings, including heart failure; however, there are few data on the role of regulatory proteins in the pathogenesis of heart failure, although a few interesting hypotheses have been proposed. A considerable body of evidence favours the view that alteration of the myocardial thin filament is the primary event leading to defective contractility of the failing myocardium, while the changes in Ca(2+) handling are a compensatory response. A better understanding of the role of regulatory proteins under different physiological and pathological conditions could lead to new therapeutic approaches in heart failure. Recently, calcium sensitisation has been proposed as a novel method by which cardiac performance may be enhanced via an increase in the affinity of troponin C for calcium but without affecting intracellular calcium concentration. To date, the only calcium sensitizer used in clinical practice is levosimendan.
OBJECTIVES: To evaluate the accuracy of B-type natriuretic peptide levels (BNP) in the diagnosis of heart failure and left ventricular dysfunction. DATA SOURCES: Electronic search in Medline, Embase, Cochrane Library and Medion database, and hand search of reference lists. REVIEW METHODS: We have included published studies on the accuracy of BNP which had both sufficient information to construct the 2x2 diagnostic cross table and an appropriate spectrum of patients. RESULTS: Fifty five studies (16,730 patients) were analyzed. The main determinants of diagnostic accuracy were the reference standard analyzed (clinical heart failure versus left ventricular dysfunction), and the methodological quality of the study. BNP levels were highly accurate for the diagnosis of clinical heart failure (diagnostic OR=41; 95% CI 23-74). The negative likelihood ratios were homogeneous, and useful for excluding the existence of heart failure (pooled negative likelihood ratio=0.11; 95% CI 0.08-0.16). The studies focused on the identification of left ventricular dysfunction were heterogeneous, with indications of publication bias, and showed less overall diagnostic accuracy than studies focused on heart failure. CONCLUSIONS: BNP levels are useful for ruling out heart failure. The accuracy of BNP for identifying patients with systolic dysfunction is more limited.
Sympathetic activation and sleep apnea are present in most patients with symptomatic systolic heart failure (HF). Acutely, obstructive and central apneas increase muscle sympathetic activity (MSNA) during sleep by eliciting recurrent hypoxia, hypercapnia, and arousal. In obstructive sleep apnea patients with normal systolic function, this increase persists after waking. Whether coexisting sleep apnea augments daytime MSNA in HF is unknown. We tested the hypothesis that its presence exerts additive effects on MSNA during wakefulness. Overnight sleep studies and morning MSNA recordings were performed on 60 subjects with ejection fraction <45%. Of these, 43 had an apnea-hypopnea index > or =15 per hour. Subjects with and subjects without sleep apnea were similar for age, ejection fraction, HF etiology, body mass index, blood pressure, and heart rate. Daytime MSNA was significantly higher in those with sleep apnea (76+/-2 versus 63+/-4 bursts per 100 heartbeats [mean+/-SEM], P=0.005; 58+/-2 versus 50+/-3 bursts/min, P=0.037), irrespective of its etiology (the mean difference for central sleep apnea was 17 bursts per 100 heartbeats; n=14; P=0.006; and for obstructive sleep apnea, 11 bursts per 100 heartbeats; n=29; P=0.032). In a subgroup (n=8), treatment of obstructive sleep apnea lowered MSNA by 12 bursts per 100 heartbeats (P=0.003). Convergence of independent excitatory influences of HF and sleep apnea on central sympathetic neurons results in higher MSNA during wakefulness in HF patients with coexisting sleep apnea. This additional stimulus to central sympathetic outflow may accelerate the progression of HF; its attenuation by treatment of sleep apnea represents a novel nonpharmacological opportunity.