AbstractCardiac physiologic pacing (CPP), encompassing cardiac resynchronization therapy (CRT) and conduction system pacing (CSP), has emerged as a pacing therapy strategy that may mitigate or prevent the development of heart failure (HF) in patients with ventricular dyssynchrony or pacing‐induced cardiomyopathy. This clinical practice guideline is intended to provide guidance on indications for CRT for HF therapy and CPP in patients with pacemaker indications or HF, patient selection, pre‐procedure evaluation and preparation, implant procedure management, follow‐up evaluation and optimization of CPP response, and use in pediatric populations. Gaps in knowledge, pointing to new directions for future research, are also identified.
The Modulating Effects of Cardiac Resynchronization Therapy on Myocardial Metabolism in Heart Failure
Heart failure (HF) is associated with changes in cardiac substrate utilization and energy metabolism, including a decline in high‐energy phosphate content, mitochondrial dysfunction, and phosphotransfer enzyme deficiency. A shift toward glucose metabolism was noted in the end stage of HF in animals, although HF in humans may not be associated with a shift toward predominant glucose utilization. Deficiencies of micronutrients are well‐established causes of cardiomyopathy. Correction of these deficits can improve heart function. The genes governing the energy metabolism were predominantly underexpressed in nonischemic cardiomyopathy and hypertrophic cardiomyopathy but were overexpressed in ischemic cardiomyopathy. Cardiac resynchronization therapy (CRT) has been proven to increase cardiac efficiency without increasing myocardial oxygen consumption. Altered myocardial metabolism is normalized by CRT to improve ventricular function.
Cardiac Troponin T (TNNT2) Mutations in Chinese Dilated Cardiomyopathy Patients
Background. Dilated cardiomyopathy (DCM) is one of the leading causes of heart failure with high morbidity and mortality. Although more than 40 genes have been reported to cause DCM, the role of genetic testing in clinical practice is not well defined. Mutations in the troponin T (TNNT2) gene represent an important subset of known disease-causing mutations associated with DCM. Therefore, the aim of the present study was to determine the genetic variations inTNNT2and the associations of those variations with DCM in Chinese patients.Methods. An approximately 4 kb fragment of theTNNT2gene was isolated from 103 DCM patients and 192 healthy controls and was analyzed by DNA sequence analysis for genetic variations.Results. A total of 6TNNT2mutations were identified in 99 patients, including a G321T missense mutation (Leu84Phe) and 5 novel intronic mutations. Alleles of two novel SNPs (c.192+353C>A, OR=0.095, 95% CI:0.013–0.714,P=0.022; c.192+463G>A, OR=0.090, 95% CI:0.012–0.675,P=0.019) and SNP rs3729843 (OR=1.889, 95% CI:1.252–2.852;P=0.002) were significantly correlated with DCM.Conclusions. These results suggest that the missense mutation (Leu84Phe) and two novel SNPs (c.192+353C>A, c.192+463G>A) inTNNT2gene might be associated with DCM in the Chinese population.