br Heart rate turbulence HRT HRT was introduced by Schidmt

Heart rate turbulence (HRT) HRT was introduced by Schidmt in 1999 [11]. It refers to the physiological phenomenon in response to a premature beat. After a ventricular premature contraction (VPC) and a compensatory pause, there is an increase in blood pressure because of the prolonged filling. Reflex parasympathetic activation accelerates and then slows down the osthole rate, which eventually returns to normal. The relative change in RR intervals before and after the VPC is defined as HRT onset (TO), and the slope of that regression is defined as the turbulence slope (TS). To date, HRT has been examined mainly in post-MI patients, and it is suggested that abnormal HRT is associated with increased mortality after MI [11,47,48]. A large prospective study validated HRT in post-MI patients. In that study, 1455 survivors of an acute MI in sinus rhythm were enrolled, and TO and TS were calculated from Holter monitoring. Multivariate analysis showed that the presence of both abnormal TO and TS was the strongest predictor of death (hazard ratio, 5.9; 95% CI, 2.9–12.2). It was concluded that HRT is a strong predictor of subsequent death in post-MI patients of the reperfusion era [49]. Although HRT is currently regarded as a strong predictor of mortality and malignant ventricular arrhythmia after MI, the available evidence is insufficient to support the routine use of HRT testing in post-MI patients. Further studies are necessary to establish its clinical utility in risk stratification.
Newly developed noninvasive techniques Deceleration capacity (DC) is a new risk stratifier, which is based on the assessment of deceleration-related modulations of heart rate and is considered to reflect the vagal activity of the autonomic nervous system. It was introduced by Bauer et al. in 2006 by using a signal-processing algorithm to separately characterize the deceleration and acceleration of heart rate [50]. They demonstrated that an impaired heart rate DC is a powerful predictor of mortality after MI and is more accurate than LVEF and the conventional measures of HRV. Wavelet transform analysis is a novel time–frequency technique that detects transient changes in an ECG even if they are superimposed on the high-gain QRS complex. High-frequency components in the QRS complex detected by this technique are considered to reflect conduction abnormality hidden within the QRS complex, which may be responsible for malignant ventricular arrhythmias. Previously, Morlet et al. developed a wavelet-transformed ECG for the detection of patients at risk of VT. They found that detection of local conduction abnormality in the QRS complex by wavelet transform was useful for VT risk stratification in post-infarction patients and reported 85% specificity and 90% sensitivity for VT detection [51]. Recently, we evaluated the utility of a wavelet-transformed ECG in post-MI patients. The sensitivity of the abnormal high-frequency components within the QRS complex for identifying VT/VF patients was higher than that of SAECG (96% versus 72%), although the specificity was similar (68.5% versus 64.3%) [44]. Furthermore, Tsutsumi et al. suggested that the combined use of LPs and intra-QRS high-frequency potentials hidden within the QRS complex improved the prediction of lethal ventricular arrhythmias in post-MI patients [52].
Conclusions
Disclosures
Conflict of interest
Financial support
Introduction The implantable cardioverter-defibrillator (ICD) improves survival in patients with a history of ventricular tachyarrhythmias (VTAs) or those with heart failure (HF) and depressed left ventricular function [1–4]. Despite this survival advantage, an important prognostic association between ICD shocks for VTAs and adverse outcomes has been demonstrated. Patients receiving an ICD shock for a spontaneous VTA are at increased risk of death [5,6]. Patients with more ICD-shocked VTA episodes have a higher risk of death than patients with less [6]. Electrical storm, a syndrome characterized by frequent ICD shocks for multiple VTA episodes over a short period, has more serious prognostic consequences than VTAs unrelated to electrical storm [7]. Electrical storm survivors are at high risk of early death during the first 3 months after the phenomenon [8,9]. These deaths after ICD shocks for VTAs are commonly related to progressive HF [5,6,8–11]. The association of shocked VTAs, HF, and mortality is clear, although the underlying mechanisms remain uncertain. While VTA episodes may be a marker for high-risk patients, there is the possibility that harmful effects of VTAs, shocks, and their combination are involved in HF progression and associated mortality. Some investigators have speculated that ICD shocks for VTAs may activate signaling pathways in the molecular cascade of HF [7,8,12,13]. We recently created a chronic animal model of ventricular fibrillation (VF) storm in which left ventricular function deteriorated along with striking activation of the intracellular Ca2+-sensitive phosphorylating enzyme Ca2+/calmodulin-dependent protein kinase II (CaMKII) [14], a validated signaling molecule causing HF. The aim of this paper is to discuss the potential roles of shocks and VTAs in HF progression and to present our proposal that CaMKII could connect shocked VTAs to adverse outcomes.