Pacemaker dependency and conduction system recovery following transcatheter aortic valve implantation.

BACKGROUND: Transcatheter aortic valve implantation (TAVI)-related conduction system disorders are dynamic and may resolve over time. The purpose of this study was to investigate predictive factors of PM dependency among patients receiving permanent PM implantation after TAVI. METHODS: We included 37 consecutive patients who underwent PPM implantation within six days after TAVI and who completed a 12-month follow-up. Patients were divided into two groups according to PPM dependency at follow-up: PPM-dependent group and non-PPM-dependent group. Device follow-ups were performed at one, six and 12 months. RESULTS: There were no significant differences in either baseline clinical characteristics or procedural data and results. Analysis of baseline ECGs showed a statistical difference in PR interval (200.1±17.2 ms in the PPM-dependent group vs. 175±23.3 ms in the non PPM-dependent group [P=0,003]) and in the presence of RBBB (four patients in the PPM-dependent group vs. no patients in the non PPM-dependent group [P=0.02]) as well as QRS duration (117.3±27.4 ms in the PPM-dependent group and 99±18.3 msec in the non PPM-dependent group [P=0.04]). CONCLUSIONS: The rate of PPM dependency was significantly reduced at 12-month follow-up: from 62,2% at the time of implantation to 35,1%. PR interval and RBBB were the most important predictive factors for PPM dependency. Persistent AVB and alternating BBB were prevalent in the PPM-dependent group. In the absence of persistent AVB or alternating BBB, we suggest that patients without long PR interval and RBBB at baseline ECG be carefully evaluated before permanent PM implantation, as conduction system recovery is possible.

Acute myocardial infarction in a patient with MELAS syndrome: a possible link?

The mitochondrial encephalomyopathy, lactic acidosis, and stroke (MELAS) syndrome is a mitochondrial disorder, commonly caused by m.3243A>G mutation in the MT-TL1 gene. It encodes for the mitochondrial leucine transfer RNA (tRNA Leu [UUR]), implicated in the translation of proteins involved in the assembly and function of mitochondrial complexes in the electron transport chain. The m.3243A>G mutation determines complex I (CI) deficiency, ultimately leading to NADH accumulation, higher rates of glycolysis in order to compensate for the reduced ATP production and increase in lactates, the end-product of glycolysis. Disruption of the oxidative phosphorylation function with an inability to produce sufficient energy results in multi-organ dysfunction, with high energy demanding cells, such as myocytes and neurons, being the most affected ones. Therefore, MELAS syndrome is characterized by a heterogeneous clinical spectrum. Here we report on a case of a 55-year-old man affected by MELA syndrome with no cardiovascular risk factors. He was admitted to our department because of a non ST-segment elevation myocardial infarction (NSTEMI). A coronary angioplasty of the posterior descending artery and of the left anterior descending artery was realized. Transthoracic echocardiography showed inferior and anterior left ventricular wall hypokinesis together with a moderate left ventricle hypertrophy. Cardiac involvement is reported in about a third of the patients and left ventricular hypertrophy (LVH) is the most common phenotype, with possible dilated cardiomyopathy in end-stage disease; brady- arrhythmias and tachy-arrhythmias are also frequently reported as well as Wolff- Parkinson-White (WPW) syndrome. Organ impairment and clinical manifestations depend on the heteroplasmy level of mutant DNA in cells that can differ among individuals, explaining why some patients present a more severe disease. A clear relationship between MELAS syndrome and atherosclerosis has never been established, however recently advocated. In vitro studies in MELAS patients have shown that higher mitochondrial ROS levels and increased expression of oxidative stress-related genes, as a consequence of complex I deficiency and disrupted electron transport, allow circulating LDL to be promptly oxidized into ox-LDL, contributing to endothelial dysfunction and atherosclerosis plaque formation. In light of the recent evidence suggesting a possible link between mitochondrial disorders and atherosclerosis, we speculate that MELAS syndrome may have played a role in the pathogenesis of coronary artery disease in our patient. Further investigations are needed to confirm a pathogenetic link.