Background and Objectives Significant rather than moderate coronary artery stenosis has been postulated to be the main substrate of plaque rupture in acute myocardial infarction (AMI). We evaluate if cavitation could influence the coronary artery plaque rupture contributing to the progression of thrombotic process. Methods We reconstructed a 3D model of the left anterior descending coronary artery (LAD) after reviewing the intravascular ultrasound (IVUS) data of 30 consecutive patients with mild to severe coronary artery disease. Results Turbulent flow or cavitation occurs in both concentric and eccentric coronary artery stenosis (≥ 75% for the former and ≥ 50% for the latter). The analysis of vapor phase demonstrated that cavitation propagated downstream, creating microbubbles, which exploded when the fluid pressure was lower than the vapor pressure at a local thermodynamic state. The relative higher vorticity magnitude (as turbulent flow in vivo angiogram) observed on the distal cap of the atherosclerotic plaque created a higher turbulence, probably able to destabilize the plaque through a micro-erosion process. Conclusions Cavitation seems to be able to promote the thrombotic occlusion within the coronary vessels due the ‘constant injuries’ created by the micro-explosion of bubbles.

Background: This study aimed to evaluate serum lipoprotein(a) concentrations in Vietnamese patients with acute myocardial infarction and to investigate the relationship between high serum concentrations of lipoprotein(a) and major adverse cardiovascular events after acute myocardial infarction. Methods: We conducted a prospective cohort study that included data from 199 patients with acute myocardial infarction admitted to the Cardiology Department, Cho Ray Hospital, Vietnam. Data on demographics, and hematologic, and biochemical blood test results, including serum lipoprotein(a) concentrations and coronary angiography results, were collected. All major cardiovascular adverse events (MACE) were defined as cardiovascular mortality, non-fatal myocardial infarction, and non-fatal ischemic stroke in hospital 30 days after discharge. Results: In patients with acute myocardial infarction, serum concentrations of lipoprotein(a) were not normally distributed, and skewed to the right, with a median of 17.8 mg/dL, interquartile range (IQR) 7.6-34.5 mg/dL. Overall, 29.1%, 17.1%, 12.6%, and 6.5% of patients had a serum lipoprotein(a) concentration of ≥ 30, ≥ 50, ≥ 70, and ≥ 90 mg/dL, respectively. Patients with a serum lipoprotein(a) concentration of ≥ 50 mg/dL had a higher BMI (p = 0.04), a higher rate of non-ST-elevation myocardial infarction (NSTEMI) (p = 0.035), a lower GRACE score (p = 0.038), higher levels of total cholesterol, high-density lipoprotein cholesterol (HDL-C) and unadjusted low-density lipoprotein cholesterol (LDL-C) concentrations (p = 0.002, 0.015, < 0.001, respectively), and a higher rate of three-vessel disease (p = 0.023) compared to patients with a serum lipoprotein(a) concentration < 50 mg/dL. The relative risk between lipoprotein(a) ≥ 50 mg/dL and MACE was 2.37. Conclusions: Patients with acute myocardial infarction and serum lipoprotein(a) ≥ 50 mg/dL were more likely to have NSTEMI and a lower GRACE score. Lipoprotein(a) ≥ 50 mg/dL at the time of acute myocardial infarction was not associated with in-hospital MACE, 30-days-after-discharge MACE, nor with all-cause mortality within 6 months of study follow-up.

Background. The differential diagnosis of chest pain in women is complex, ranging from atypical angina to chest pain in the absence of coronary artery disease (i.e., Syndrome X). The mechanism of these conditions remains unexplained. The purpose of this study was to examine coronary blood flow based on a new angiographic technique. Methods. Patients with chest pain were enrolled. In the new technique, as the contrast injection stopped, the blood in white color moved in and displaced the black contrast. Characteristics of blood flow could be observed and classified by type and time. The duration of the arterial phase was calculated and compared with the control. Results. Sixty patients were enrolled. Ten patients with normal coronary arteries and ventricular function; without chest pain served as controls. In the control group, the duration of the arterial phase in the RCA was 1.76 sec, while it was 3.76 sec for the syndrome X group (p<0.05). From the mMID segment to the distal segment, syndrome X patients had a much longer delay compared to control subjects (0.81 vs. 0.26 sec) (p<0.05). From the distal segment (bDIS) to the origin of the PDA, syndrome X patients had an average duration of 0.81 sec compared to 0.40 sec in controls (p<0.05). The largest difference was the period of time when the contrast left the PDA until flushed from the distal vasculature, which was 1.66 sec and 0.40 sec in syndrome X vs. control. Syndrome X patients with prolonged myocardial phase (1.89 sec) had dense and prolonged contrast retention at the myocardium. Conclusions. In patients with syndrome X, the prolonged arterial phase deprived the myocardium of highly oxygenated blood and triggered ischemia. This new imaging method allows for a better understanding of the mechanism of ischemia in Syndrome X patients.