In this study, it has been demonstrated that low-dose ICSK given immediately after primary PCI significantly limits long-term infarct size and preserves left ventricular volumes and functions. (Effect of Complementary Intracoronary Streptokinase Administration Immediately After Primary Percutaneous Coronary Intervention on Microvascular Perfusion and Late Term Infarct Size in Patients With Acute Myocardial Infarction; NCT00302419).
BackgroundThe contribution of functionally disturbed coronary autoregulation and structurally impaired microvascular vasodilatory function to reduced coronary flow velocity reserve, reflecting impaired coronary microcirculation in diabetes mellitus (DM), has not been clearly elucidated. The objective of this study was to identify the mechanism of coronary microvascular impairment in DM in relation to duration of disease.Methods and ResultsCoronary flow velocities in the anterior descending coronary artery were assessed by transthoracic echocardiography following angiography revealing normal epicardial coronary arteries in 55 diabetic and 47 nondiabetic patients. Average peak flow velocities, coronary flow velocity reserve, and microvascular resistance in baseline and hyperemic conditions (baseline and hyperemic microvascular resistance, respectively) were assessed. Reduced coronary flow velocity reserve in patients with short duration (<10 years) of DM compared with nondiabetic patients was primarily driven by increased baseline average peak flow velocity (26.50±5.6 versus 22.08±4.31, P=0.008) in the presence of decreased baseline microvascular resistance (3.69±0.86 versus 4.34±0.76, P=0.003). In contrast, decreased coronary flow velocity reserve in patients with long‐standing (≥10 years) DM compared with nondiabetic patients was predominantly driven by reduced hyperemic average peak flow velocity (41.57±10.01 versus 53.47±11.8, P<0.001) due to increased hyperemic microvascular resistance (2.13±0.42 versus 1.69±0.39, P<0.001).ConclusionsBoth altered coronary autoregulation and impaired microvascular vasodilatory function contribute to DM‐related coronary microvascular impairment in a time‐dependent manner. DM‐induced early functional microvascular autoregulatory impairment seems to evolve into structural microvascular impairment in the initially overperfused microvascular territory at the later stage of disease.
Background
Although ST-segment elevation (STE) has been used synonymously with acute coronary occlusion (ACO), current STE criteria miss nearly one-third of ACO and result in a substantial amount of false catheterization laboratory activations. As many other electrocardiographic (ECG) findings can reliably indicate ACO, we sought whether a new ACO/non-ACO myocardial infarction (MI) paradigm would result in better identification of the patients who need acute reperfusion therapy.
Methods
A total of 3000 patients were enrolled in STEMI, non-STEMI and control groups. All ECGs were reviewed by two cardiologists, blinded to any outcomes, for the current STEMI criteria and other subtle signs. A combined ACO endpoint was composed of peak troponin level, troponin rise within the first 24 h and angiographic appearance. The dead or alive status was checked from hospital records and from the electronic national database.
Results
In non-STEMI group, 28.2% of the patients were re-classified by the ECG reviewers as having ACO. This subgroup had a higher frequency of ACO, myocardial damage, and both in-hospital and long-term mortality compared to non-STEMI group. A prospective ACOMI/non-ACOMI approach to the ECG had superior diagnostic accuracy compared to the STE/non-STEMI approach in the prediction of ACO and long-term mortality. In Cox-regression analysis early intervention in patients with non-ACO-predicting ECGs was associated with a higher long-term mortality.
Conclusions
We believe that it is time for a new paradigm shift from the STEMI/non-STEMI to the ACOMI/non-ACOMI in the acute management of MI. (DIFOCCULT study; ClinicalTrials.gov number, NCT04022668.)
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