STEMI Marked by Microvascular Dysfunction Linked to Higher Long-term Mortality

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Microvascular dysfunction, measured by Doppler flow velocity measurements after primary percutaneous coronary intervention (PCI), is associated with increased long-term mortality in patients with anterior-wall ST-segment elevation myocardial infarction (STEMI). The single-center, retrospective analysis was published online June 4, 2013, ahead of print in Circulation: Cardiovascular Interventions.

Researchers led by Jan J. Piek, MD, PhD, of Academic Medical Center (Amsterdam, The Netherlands), looked at 100 consecutive patients at their institution with a first anterior wall STEMI. Intracoronary blood flow velocity in the infarct-related artery was measured 5 to 10 minutes after successful PCI. The researchers used a 0.014-inch Doppler-sensor equipped guidewire (Volcano, San Diego, CA), to determine coronary flow velocity reserve (CFVR).

Complete follow-up was obtained in 94 of the patients, with TIMI 3 flow achieved in 75% and myocardial blush grade 3 achieved in 52% by the end of the procedure. Mean CFVR in the infarct-related artery was 1.6 ± 0.4 compared with 2.4 ± 0.5 in the reference vessel. A rapid diastolic deceleration time (DDT < 600 ms) was found in just over half of patients (52%), and early systolic retrograde flow was present in under a third (29%).

CFVR Cutoff Values Defined

The 10-year Kaplan-Meier cumulative all-cause mortality estimate was 15%, with a 10-year cardiac mortality of 14%. The optimal identified cutoff values were 2.1 for CFVR in the reference vessel (sensitivity 73%, specificity 71%) and 1.5 for CFVR in the infarct-related artery (sensitivity 73%, specificity 62%).

Ten-year estimates of cardiac mortality differed significantly between high- and low-reference vessel CFVR groups, ranging from 5% in patients with high-reference vessel CFVR values to 31% in patients with low-reference vessel CFVR values (P = 0.001). In contrast, 10-year estimates of cardiac mortality were not significantly different between groups (P = 0.10).

In bivariate analysis, a reference vessel CFVR of < 2.1 was associated with a 3.67-fold increase in long-term cardiac mortality risk. No such association was seen for target-vessel CFVR of < 1.5 (table 1).

Table 1. CFVR in Reference, Target Vessel and Long-term Cardiac Mortality

Variable

HR

95% CI

P Value

Reference Vessel CFVR < 2.1

3.67

1.19-11.37

0.02

Infarct-Related Artery CFVR < 1.5

1.67

0.56-4.98

0.36


There was no difference in cardiac mortality rates between patients with and without rapid DDT or systolic retrograde flow in the infarct-related artery.

After adjustment for multiple variables associated with long-term cardiac mortality, a reference vessel CFVR of < 2.1 was associated with a 4.09-fold increase in long-term cardiac mortality (P = 0.03). A persistently impaired reference vessel CFVR at 6-month follow-up (defined as a reference vessel CFVR of ≤ 2.7) was associated with over a tenfold increase in cardiac mortality during subsequent follow-up after adjustment for other variables associated with cardiac morality (P = 0.02).

“The present study is the first to indicate that . . . altered microvascular function at regions remote from the infarct-related artery is independently associated with long-term fatal cardiac events,” Dr. Piek and colleagues write.

They add that there was an “unequivocal relationship” between impaired microvascular function in a reference coronary artery and long-term fatal cardiac events, independent of LV function.

“We conclude that microvascular function, as assessed by the coronary vasodilator reserve in a reference vessel, plays a pivotal role in long-term cardiac mortality after primary PCI for STEMI,” the authors write.

Global Nature of Microvascular Dysfunction Cited

In an accompanying editorial, Andy S.C. Yong, MBBS, PhD, and William F. Fearon, MD, both of Stanford University Medical Center (Stanford, CA), note that 35% of patients in the study had a CFVR cutoff value below 2.1 in the nonculprit vessel.

“The implications of the findings are that microvascular dysfunction in the setting of STEMI can be global, and may not only involve the infarct-related territory,” they note.

Drs. Yong and Fearon acknowledge the single-center, retrospective nature of the study, but also cite the potential implications of the findings. “Whether routine assessment of the nonculprit microvascular territory is warranted will require further study,” they say. “Incorporating the assessment of the coronary microcirculation into the management algorithm in patients with STEMI could potentially provide a new paradigm in the hope of benefiting these patients.”

 


Sources:1. van de Hoef TP, Bax M, Meuwissen M, et al. Impact of coronary microvascular function on long-term cardiac mortality in patients with acute ST-segment elevation myocardial infarction. Circ Cardiovasc Interv. 2013;Epub ahead of print.

2. Yong ASC, Fearon WF. Coronary microvascular dysfunction after ST-segment-elevation myocardial infarction: Local or global phenomenon [editorial]? Circ Cardiovasc Interv. 2013;Epub ahead of print.

 

 

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Disclosures
  • Drs. Piek and Yong report no relevant conflicts of interest.
  • The editorial was supported in part by a grant from the National Institutes of Health, Heart Lung, and Blood Institute.
  • Dr. Fearon reports receiving institutional research support from St. Jude Medical.

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