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[Abnormal local ventricular electrogram and its relation to induction of ventricular tachycardia in patients with
S Miyajima1, Y Aizawa, M Satoh
1First Department of Internal Medicine, Niigata University School of Medicine.
Insights
Hypertrophic cardiomyopathy (HCM) patients exhibit prolonged local ventricular electrograms (LVE) during pacing, increasing ventricular tachycardia (VT) risk. Critical LVE prolongation at pacing sites precedes VT induction in HCM.
Area of Science:
- Cardiology
- Electrophysiology
- Medical Research
Context:
- Hypertrophic cardiomyopathy (HCM) is a genetic heart condition.
- Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia.
- Understanding VT mechanisms in HCM is crucial for patient management.
Purpose:
- To investigate the electrophysiological mechanisms underlying VT induction in HCM patients.
- To analyze local ventricular electrograms (LVE) at pacing sites in HCM patients and controls.
Summary:
- Patients with HCM showed significantly longer LVE durations compared to controls.
- Prolonged LVE at pacing sites correlated with inducible VT in HCM.
- Critical LVE prolongation preceded VT initiation, sometimes spanning the entire cardiac cycle.
Impact:
- This study elucidates a key mechanism for VT in HCM.
- Findings may inform risk stratification and therapeutic strategies for HCM patients.
- Highlights the importance of LVE analysis in predicting VT events.
Abstract:
To investigate the mechanism of induction of ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM), we reviewed and analyzed the local ventricular electrograms (LVE) at the pacing sites in 15 patients with HCM and 52 control subjects. Each patient had a clinical history of nonsustained VT or syncope. The results were as follows: 1. Rapid and polymorphic VT was induced in six of the 15 patients with HCM and in 10 of the 52 control subjects. 2. The duration of the LVE at the pacing site was progressively prolonged as the number of extrastimuli were increased or the premature intervals were shortened. Compared with the controls, patients with HCM had longer durations of the LVE by basic drive, single extrastimulus, and by double extrastimuli: 113 +/- 31 vs 95 +/- 16 ms (p less than 0.005), 156 +/- 35 vs 109 +/- 17 ms (p less than 0.001), and 220 +/- 88 vs 133 +/- 25 ms (p less than 0.001), respectively. 3. In the HCM group, the maximum duration of the LVE by double ventricular extrastimuli was significantly longer in patients with inducible VT compared with those with non-inducible VT: 287 +/- 95 vs 183 +/- 56 ms (p less than 0.05). 4. Induction of VT in the HCM group was accompanied by the critical prolongation of the LVE at the pacing site. In two of the six patients with HCM, the LVE at the pacing site spanned the entire cardiac cycle at the time of the initiation of VT.(ABSTRACT TRUNCATED AT 250 WORDS)