Exercise-induced ventricular tachycardia undergoes ischemia evaluation; however, it is important to identify idiopathic ventricular tachycardia in patients with concomitant coronary artery disease and radiofrequency ablations can be lifesaving. We report a case of exercise-induced right and left ventricular outflow tract ventricular tachycardia in a patient with triple vessel coronary artery disease.

The left main disease is significant stenosis of the left coronary artery, which is responsible of supplying blood to a major portion of the left ventricle. In this report, we describe a unique case of critical left main disease with a special clinical presentation. A 66-year-old male with insignificant past medical history presented with dyspepsia. Patient presented twice to the emergency department seeking for help for his persistent complaint. During his second visit, patient was diagnosed with type one myocardial infarction and underwent coronary angiography which showed 90% stenosis in the left main coronary artery. Patient underwent successful coronary artery bypass grafting and was sent home. This case is a unique representation of type 1 myocardial infarction as the peak troponin I level does not correlate with the extent of the myocardium being jeopardized. A big portion of the heart is at risk of injury with the 90% stenosis found in this patient\'s left main coronary artery, yet the peak troponin I level is minimum. This report provides a possible explanation of the discrepancy between the peak troponin I level and the extent of the myocardium being jeopardized and describes a common yet easily missed clinical presentation of acute coronary syndrome. Left main disease is a relatively uncommon presentation of acute coronary syndrome, with potentially serious detrimental consequences. Discrepancies do occur among patients of critical left main disease, and promptly diagnosing and managing is of great importance.

Indoleamine 2,3 dioxygenase (IDO), the rate-limiting enzyme in the kynurenine (Kyn) pathway of tryptophan (Trp) degradation, is modulated by inflammation, and is regarded as a key molecule driving immunotolerance and immunosuppressive mechanisms. Little is known about IDO activity in patients with active coronary artery disease (CAD).
We prospectively enrolled patients who were scheduled to undergo coronary angiography. Measurement of IDO, high-sensitivity troponin T (hs-TnT), and high-sensitivity C-reactive protein (hs-CRP) levels was performed at baseline, and IDO activity was monitored at the 6-month follow-up.
Three hundred and five patients were enrolled. Ninety-eight patients (32.1%) presented with recent acute coronary syndrome (ACS). Significant difference in IDO, kynurenine, and hs-TnT between patients with and without significant CAD was observed. Baseline IDO activity, kynurenine level, and hs-TnT level were all significantly higher in significant CAD patients with 3-vessel, 2-vessel, and 1-vessel involvement than in those with insignificant CAD [(0.17, 0.13, and 0.16 vs. 0.03, respectively; p = 0.003), (5.89, 4.58, and 5.24 vs. 2.74 µM/g, respectively; p = 0.011), and (18.27, 12.22, and 12.86 vs. 10.89 mg/dL, respectively; p < 0.001)]. One-year mortality was 3.9%. When we compared between patients who survived and patients who died, we found a significantly lower prevalence of left main (LM) disease by coronary angiogram (6.1% vs. 33.3%, p = 0.007), and also a trend toward higher baseline kynurenine (5.07 vs. 0.79 µM/g, p = 0.082) and higher IDO (0.15 vs. 0.02, p = 0.081) in patients who survived.
Immunometabolic response mediated via IDO function was enhanced in patients with CAD, and correlated with the extent and severity of disease. Patients with LM disease had higher 1-year mortality. Lower level of IDO, as suggested by inadequate IDO response, demonstrated a trend toward predicting 1-year mortality. Trial registration TCTR Trial registration number TCTR20200626001. Date of registration 26 June 2020. \"Retrospectively registered\".

BACKGROUND: To evaluate the accuracy of late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) and imaging stress test in predicting significant coronary artery disease (CAD) in left ventricular (LV) dysfunction.
METHODS: We enrolled 187 consecutive out-patients (61±17years) with new evidence of depressed (<45%) ejection fraction and no history of previous heart diseases and absence of Q-waves. All patients underwent coronary angiography (CA) and to LGE-CMR examination to identify ischemic and non-ischemic LGE. All patients underwent stress imaging to determine the presence of myocardial ischemia.
RESULTS: Ischemic-LGE was found in 83 patients and non-ischemic-LGE in 104. Significant CAD on CA was found in 86/187 patients. Ischemic-LGE showed a specificity of 94%, a sensitivity of 89% and an accuracy of 92% in identifying significant CAD. Imaging stress test was negative in 98/105 patients without CAD, and positive in 42/82 with significant CAD, showing a specificity of 93%, a sensitivity of 51% and an accuracy of 75% in identifying CAD. Combining CMR and stress test imaging, 94 patients had ischemic-LGE pattern and/or positive stress test for ischemia; of these 81/94 had significant CAD on CA and 13 had no CAD. Among the 93 patients with both tests negative, significant CAD was found in 5/93 patients. The combination of LGE and stress respect to only LGE did not improve the diagnostic accuracy (90 vs 92% respectively).
CONCLUSIONS: LGE-CMR had high accuracy in predicting significant CAD in ischemic LV dysfunction or as a bystander in non ischemic dysfunction.