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Effects of left ventricular dysfunction on the circadian variation of ventricular premature complexes in healed
A M Gillis1, R W Peters, L B Mitchell
1Division of Cardiology, University of Calgary, Alberta, Canada.
Insights
Severe left ventricular (LV) dysfunction abolishes the normal daily pattern of ventricular premature complexes (VPCs). This loss of circadian variation in VPCs is also seen in heart failure and with beta-blocker use.
Area of Science:
- Cardiology
- Chronobiology
- Internal Medicine
Background:
- Circadian variation in cardiovascular events is established.
- Left ventricular (LV) dysfunction impacts cardiac event timing.
Purpose of the Study:
- To evaluate the effect of LV dysfunction on circadian variation of ventricular premature complex (VPC) frequency.
- To compare VPC frequency patterns in patients with varying degrees of LV function post-myocardial infarction.
Main Methods:
- 132 patients with frequent VPCs and reduced LV function were studied.
- Patients were grouped by LV ejection fraction (LVEF ≤0.30 vs. 0.30-0.45).
- Hourly VPC frequencies and heart rates were compared; subgroup analyses included beta-blocker treatment and NYHA class.
Main Results:
- Distinct circadian variation of VPCs, including a morning peak, was present in patients with LVEF > 0.30.
- Circadian variation of VPCs was absent in patients with LVEF ≤0.30 and those with NYHA class III-IV heart failure.
- Beta-blocker treatment blunted circadian heart rate variation and abolished VPC circadian patterns.
- A positive correlation between heart rate and VPC frequency was less common in patients with LVEF ≤0.30.
Conclusions:
- Severe LV dysfunction eliminates the circadian variation of VPC frequency.
- Heart failure severity and beta-blocker therapy also disrupt VPC circadian patterns.
- These findings highlight the interplay between cardiac function, medication, and daily biological rhythms in arrhythmia occurrence.
Abstract:
Circadian variation in the onset of cardiovascular events including sudden cardiac death, myocardial infarction and ventricular arrhythmias has been described. The effect of left ventricular (LV) dysfunction on the circadian variation of ventricular premature complex (VPC) frequency was evaluated in 132 patients with frequent VPCs and reduced LV function after myocardial infarction. Patients were prospectively divided in 2 groups based on LV ejection fraction (EF) (those with LVEF less than or equal to 0.30, and those with LVEF between 0.30 and 0.45). Median hourly VPC frequencies and heart rates were compared between the 2 groups. Subgroup analyses based on treatment with beta-adrenoceptor blocking agents and on New York Heart Association functional class were also performed. In patients with LVEF greater than 0.30, a distinct circadian variation of VPCs, and the expected morning increase in VPC frequency were present. In contrast, a distinct circadian variation of VPCs was absent in patients with LVEF less than or equal to 0.30. A circadian variation of VPC frequency was also absent in patients with severe symptomatic congestive heart failure (New York Heart Association class III-IV). Treatment with beta-adrenoceptor blocking agents was associated with a loss of the circadian variation of VPC frequency. The circadian variation of heart rate was also blunted in the group treated with beta-adrenoceptor blocking agents. The proportion of subjects manifesting a positive correlation between heart rate and VPC frequency was lower in subjects with LVEF less than or equal to 0.30 (26%) than in those with LVEF greater than 0.30 (46%) (p less than 0.05). Thus, circadian variation of VPC frequency is absent in patients with severe LV dysfunction.