Electrophysiologic features of protected channels in late postinfarction patients with and without spontaneous ventricular tachycardia

Nayyar, Sachin; Wilson, Lauren; Ganesan, Anand N.; Sullivan, Thomas; Kuklik, Paweł; Young, Glenn D.; Sanders, Prashanthan; Roberts‐Thomson, Kurt C.

doi:10.1007/s10840-017-0299-6

Cited by 11 publications

(11 citation statements)

References 26 publications

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“…The dynamic responses of V MP to differential pacing can vary among patients depending on their electrophysiological differences in cell‐to‐cell conduction, and unique organization of scar‐related fixed conduction abnormalities. For instance, in cardiomyopathy patients with established VA, the activating wavefront has relatively fewer entrances to access the protected surviving myocyte network of the heterogeneous scar region . There is a high probability that a new external source of activation will engage the deep channels through the same entrance in the fibrotic scar, and the deep V MP vectors remain relatively unchanged despite altered external activation.…”

Section: Discussionmentioning

confidence: 99%

“…For instance, in cardiomyopathy patients with established VA, the activating wavefront has relatively fewer entrances to access the protected surviving myocyte network of the heterogeneous scar region. 2,22 There is a high probability that a new external source of activation will engage the deep channels through the same entrance in the fibrotic scar, and the deep V MP vectors remain relatively unchanged despite altered external activation. Moreover, many long channels or those with long refractory period are prone to complete conduction block and loss of V MP at a rapid activation rate.…”

Section: Mechanistic Basis Of Differential Pacing: Functional Versus mentioning

confidence: 99%

“…Patients with cardiomyopathy and electrical instability, manifesting as ventricular arrhythmias (VA), have greater heterogeneous scar burden, with slower conducting myocyte channels and wide fragmented intracardiac ventricular myopotentials (V MP ), all suggesting greater conduction remodeling than those without VA. 1,2 Several studies in patients with a history of VA have also shown dynamic responses of these intracardiac V MP to right-ventricular (RV) pacing (RVP). [3][4][5] The severity of this arrhythmogenic substrate is also reflected in its greater surface QRS-fragmentation and post-QRS late potentials on the signal-averaged electrocardiogram (SAECG) in sinus rhythm.…”

Section: Introductionmentioning

confidence: 99%

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Differential pacing from two sites to diagnose risk of ventricular arrhythmia and death

Nayyar

Kuklik

Tomlinson

et al. 2018

Pacing Clinical Electrophis

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Background QRS abnormalities may not be apparent in sinus rhythm in electrically stable cardiomyopathy patients who can have quiescent but highly arrhythmogenic substrate. Here, we test the hypothesis that differential changes in QRS construction during right‐ventricular apex pacing (RVP) as opposed to atrial pacing (AP) will identify latent substrate for ventricular arrhythmias (VA) and death. Methods Forty patients with cardiomyopathy free of VA underwent baseline 114‐electrode body‐surface electrocardiogram during AP (100 beats per minute [bpm]) and RVP (100 and 120 bpm). The filtered‐averaged QRS at each electrode was deconstructed into individual intra‐QRS and post‐QRS ventricular myopotentials (VMP). The primary outcome was VA or death. Prognostic accuracy of VMP was validated using V1 to V6 leads in another prospective cohort of 44‐cardiomyopathy patients. Results Twenty‐six patients were eligible for initial analysis. After 5 ± 2 years of follow‐up, eight (31%) patients had VA (VAPos) while rest were uneventful (VANeg). During AP100, VAPos patients expressed more VMP than VANeg patients (16 ± 1 vs 12 ± 1, P = 0.02). RVP100 and RVP120 in VAPos patients introduced an additional 5.5 ± 0.5 and 6.0 ± 0.5 VMP (P < 0.0001 vs AP100). The relative change with RVP120 versus AP100 in VANeg patients exceeded VAPos patients by 1.2 ± 0.5 VMP (P = 0.03). Increment in VMP count of <8 in lead‐V5 with RVP120 compared to AP100 best predicted VA (area under curve 0.81, P = 0.01). In the validation cohort, primary outcome occurred in 13 (33%) patients. Native QRS features and AP100 alone failed to predict primary outcome. Patients with increment in VMP count of <8 in lead‐V5 with RVP120 versus AP100 had 7.9‐fold increased risk of primary outcome (95% confidence interval 1.01, 61.61; P = 0.049). Conclusion Cardiomyopathy patients at risk of VA or death perturb the QRS less than low‐risk patients with differential pacing. This functional response may be useful to identify arrhythmogenic substrate.

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Section: Discussionmentioning

confidence: 99%

Section: Mechanistic Basis Of Differential Pacing: Functional Versus mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Differential pacing from two sites to diagnose risk of ventricular arrhythmia and death

Nayyar

Kuklik

Tomlinson

et al. 2018

Pacing Clinical Electrophis

Self Cite

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“…The problem of postinfarction cardiosclerosis is reflected in many recent scientific papers. The basis of these studies is the study of the characteristics of hemodynamics and the state of structural geometric cardiac remodeling, neurovegetative regulation, electrophysiological signs of electrical instability, cardiac arrhythmias, dispersion of the QT interval, the presence of late ventricular potentials [1][2][3]. A number of works are devoted to the search for effective and safe methods of treatment and prevention of the above described deviations [3,4], while the use of taurine [4][5][6] is considered as a promising approach in this aspect.…”

Section: Introductionmentioning

confidence: 99%

Modern Possibilities of Metabolic Therapy in Improving the Quality of Life in Patients with Postinfarction Cardiosclerosis

Irina¹,

Vladimir²

2019

AJIM

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95 patients with postinfarction cardiosclerosis and angina pectoris II and III functional classes were examined. The study included patients who refused intervention revascularization. The main group included 48 patients who were added taurine (Dibikor 750 mg / day) to enhance the effect of basic therapy, and the comparison group included 47 patients who received standard therapy and placebo. The duration of treatment was 3 months. The study demonstrated positive effects of taurine that was confirmed by significant improvements in the following indicators: subjective status, indicators of the Seattle questionnaire, echocardiographic parameters, cardiac arrhythmias. There was a decrease in the severity of fatigue by 2 times, a decrease in the intensity of complaints of palpitations by 72.3%, a decrease in the severity of dyspnea by 30.0% and a severity of pain in the heart area by 50%. Indicators of most scales of the Seattle questionnaire in patients of the main group at the end of the study significantly exceeded (p <0.05) the corresponding values in patients of the comparison group. In patients whose treatment was used taurine, a significant improvement in inotropic function was noted (the ejection fraction is significantly higher than in the comparison group, respectively 56.0 ± 1.8 and 53.5 ± 1.1%, p <0,05), the bathmotropic and chronotropic myocardial functions improved, which was shown by a 45% decrease in the number of ventricular extrasystoles, a 57% decrease in the frequency of supraventricular heart rhythm disturbances, a decrease in the incidence rate of ST segment depression (in the main group the number of episodes was significantly lower than p <0,05 than in the comparison group). The use of taurine in the complex treatment of patients with exertional angina, after suffering a myocardial infarction, is safe and not accompanied by side effects. Taurine is advisable to include in the complex treatment of patients with exertional angina pectoris, who have had a myocardial infarction in order to improve the myocardial inotropic function, enhance the antiarrhythmic and lipid-lowering effects of the basic therapy. The recommended dose of Taurine is 750 mg per day as a supplement to standard therapy with a duration of therapy of at least 3 months.

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“…Проблема постинфарктного кардиосклероза отражена во многих научных работах последнего времени. Основой этих исследований является изучение особенностей гемодинамики и состояния структурногеометрического ремоделирования сердца, нейровегетативной регуляции, электрофизиологических признаков электрической нестабильности мио-карда -нарушения сердечного ритма, дисперсии интервала QT, наличия поздних потенциалов желудочков [1][2][3]. Ряд работ посвящен поиску эффективных и безопасных методов лечения и профилактики вышеописанных отклонений [3,4], при этом в качестве перспективного подхода в этом аспекте рассматривается применение таурина [4][5][6].…”

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TAURIN INFLUENCE ON CLINICAL COURSE OF STAbLE ANGINA IN POSTINFARCTION CARDIOSCLEROSIS PATIENTS

Vasilieva

Резван

2018

Russ J Cardiol

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Aim. Study of efficacy and safety of taurin in management of stable angina patients with postinfarction cardiosclerosis.Material and methods. Totally, 95 postinfarction cardiosclerosis patients included, with stable angina of II and III functional class. The patients that were included, had refused revascularization. To the main group, 48 were included with added taurin (Dibicor, “PIK-Pharma”, Russia, 750 mg daily), and to comparison group — 47 patients that were taking standard treatment and placebo. Treatment duration 3 months. Results. Clinical efficacy of taurin in postinfarction cardiosclerosis and stable angina is confirmed by significant improvement of the following parameters: subjective state (decreased fatigue, less complaints on palpitation, less severity of dyspnea and rarer angina attacks), of the life quality parameters by Seattle questionnaire; echocardiographic parameters, normalized cardiac rhythm. Postive changes achieved on the basis therapy with taurin, remained for 3 months after drug discontinuation.Conclusion. Positive influence of taurin on clinical and instrumental parameters of patients make it to recommend its prescription for stable angina treatment in postinfarction cardiosclerosis patients.

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Electrophysiologic features of protected channels in late postinfarction patients with and without spontaneous ventricular tachycardia

Cited by 11 publications

References 26 publications

Differential pacing from two sites to diagnose risk of ventricular arrhythmia and death

Differential pacing from two sites to diagnose risk of ventricular arrhythmia and death

Modern Possibilities of Metabolic Therapy in Improving the Quality of Life in Patients with Postinfarction Cardiosclerosis

TAURIN INFLUENCE ON CLINICAL COURSE OF STAbLE ANGINA IN POSTINFARCTION CARDIOSCLEROSIS PATIENTS

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