CHANGES IN ECG PARAMETERS IN PATHOLOGY AND UNDER THE INFLUENCE OF DRUGS

Abstract

The precise evaluation of electrocardiographic alterations induced by the synergistic interplay between underlying structural cardiomyopathies and pharmacological interventions represents a defining challenge in modern clinical electrophysiology. This investigation aims to quantitatively analyze the independent and combined effects of specific pathological substrates—namely ischemic heart disease and heart failure—and arrhythmogenic drug classes on ventricular depolarization and repolarization metrics. Executing a prospective observational cohort design, the study monitored 1850 adult patients across a 24-month clinical window. High-resolution continuous 12-lead Holter monitoring captured microvolt-level fluctuations in PR intervals, QRS duration, corrected QT intervals (QTc via Fridericia), and the transmural dispersion of repolarization (Tp-e interval). The empirical data exposed a severe amplification of proarrhythmic risk when xenobiotics interacted with compromised myocardium. Patients subjected to a "dual-hit" scenario—combining baseline ischemic pathology with I_Kr-blocking pharmacological agents (such as Class III antiarrhythmics or specific psychotropics)—exhibited an average QTc prolongation reaching 488 ± 22 ms, drastically exceeding the 410 ± 12 ms baseline observed in strictly physiological controls. Furthermore, the incidence rate of critical repolarization delays (QTc > 500 ms) surged to 14.5% in the dual-hit cohort, compared to a mere 3.2% in patients possessing structurally normal hearts exposed to identical pharmacological regimens. The Tp-e interval, a highly specific marker for arrhythmogenesis, widened by 42% in the pathological-pharmacological intersection group, strongly correlating with early afterdepolarizations. These findings definitively establish that structural pathology critically erodes the repolarization reserve. Consequently, administering standard dosages of electrophysiologically active drugs to structurally compromised patients mathematically guarantees toxic threshold breaches. The data mandates an immediate paradigm shift toward continuous, algorithm-driven electrocardiographic surveillance to preempt catastrophic ventricular arrhythmias in vulnerable clinical populations.