Intensive Early and Sustained Lowering of Non–HDL-C

Quick Takes

  • After an MI, the rates of cardiovascular outcomes and mortality were lowest among patients achieving the largest reductions in non–HDL-C and the lowest non–HDL-C levels down to ∼2 mmol/L.
  • The lowest risk was observed when non–HDL-C targets or reductions were achieved early after MI and sustained thereafter, reflecting greater use of and maintenance of more potent lipid-lowering regimens.
  • These data support earlier use of regimens capable of providing both early and sustained intensive lowering of non–HDL-C.

Study Questions:

What is the relationship between non–high-density lipoprotein cholesterol (non–HDL-C) levels after myocardial infarction (MI) and risk of adverse outcomes?

Methods:

The investigators included 56,262 patients with MI from the SWEDEHEART registry for this study. Outcomes were major adverse cardiovascular event (MACE: death, MI, and ischemic stroke), death, and nonfatal MI. Non–HDL-C was assessed at admission, 2 months, and 1 year. Target achievement (<2.2 mmol/L) of non–HDL-C, timing thereof, and outcomes were assessed. The difference in non–HDL-C between the MI hospitalization and the first and second follow-up visits was calculated. Kaplan–Meier survival probability estimates were calculated from the date of follow-up visit and to the total follow-up at 12 years for all outcomes, stratified by change in non–HDL-C.

Results:

During a median follow-up of 5.4 years, 9,549 had MACE, 5,427 died, and 3,946 had MI. Long-term hazard ratio (HR) for MACE in the lowest versus the highest quartile of achieved non–HDL-C at 1 year was 0.76 (95% confidence interval [CI], 0.71-0.81). Short-term results were consistent also when assessing non–HDL-C levels at 2 months, including early events up to 1 year (HR, 0.80; 95% CI, 0.68-0.92). Similar results were observed for all outcomes. Patients achieving both early and sustained targets had the lowest risk of outcomes (HR, 0.80; 95% CI, 0.74-0.86) versus patients achieving target early or late (HR for both, 0.86; 95% CI, 0.79-0.93).

Conclusions:

The authors report that the lowest achieved levels both at 2 months and at 1 year of non–HDL-C were associated with a better outcome.

Perspective:

This observational study investigated the potential impact of the timing and the magnitude of change in non–HDL-C levels after MI and subsequent risk of MACE, all-cause mortality, and nonfatal MI. After an MI, the rates of cardiovascular outcomes and mortality were lowest among patients achieving the largest reductions in non–HDL-C and the lowest non–HDL-C levels down to ∼2 mmol/L. The lowest risk was observed when non–HDL-C targets or reductions were achieved early after MI and sustained thereafter, reflecting greater use of and maintenance of more potent lipid-lowering regimens. These data support earlier use of regimens capable of providing both early and if maintained sustained intensive lowering of non–HDL-C. One notable limitation is the observational nature of the study, which inherently introduces potential biases and confounding factors.

Clinical Topics: Diabetes and Cardiometabolic Disease, Dyslipidemia, Prevention, Lipid Metabolism, Nonstatins, Acute Coronary Syndromes

Keywords: Cholesterol, HDL, Myocardial Infarction, Secondary Prevention


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