Magnetic resonance imaging

Cardiovascular magnetic resonance (CMR) has become an established non-invasive imaging modality for the diagnosis of coronary artery disease and contributes important information for therapeutic decisions regarding revascularization. Besides having the unparalleled versatility to provide insight on a range of diagnostic parameters such as cardiac morphology, function, myocardial texture, and vascular flow, CMR allows the detection of ischaemia and myocardial viability to guide therapeutic decisions. For the identification of ischaemia, CMR provides two basic methods, which are routinely used in clinical practice. Ischaemia can either be visualized as regional hypoperfusion when using CMR perfusion imaging during vasodilator-induced hyperaemia, or as impaired regional wall motion under dobutamine stress CMR. For the assessment of viability, the late gadolinium enhancement technique represents a sensitive CMR method to discriminate viable myocardium from irreversibly damaged myocardial scar tissue. CMR has proven its robustness, diagnostic performance, and prognostic value in patients with coronary artery disease in several multicentre trials.

P1437 Integrated ST segment elevation score as a new predictor of the myocardial scar extent determined with LGE-CMR at 1-month follow-up after STEMI

Funding Acknowledgements Funded by the research grant PlaqueImage, contract number 26/01.09.2016, SMIS code 103544, by the European Union and the Government of Romania Background The inflammatory response in the acute phase of a myocardial infarction, as well as in later phases contributes to the healing process of the infarcted myocardium and the left ventricular remodeling. Restoration and improvement of LV function highly depends on the magnitude of scar formation. Late gadolinium enhancement cardiac magnetic resonance (LGE-CMR) imaging has been validated for an accurate determination of the myocardial scar size and transmurality. The recovery of ST segment elevation is a liable marker of vessel patency following PCI. Purpose The aim of the study was to validate a new integrated score of ST segment elevation score (ISSTE) as a new predictor of the myocardial scar tissue size, in relation with increased inflammatory biomarkers, with the extent of myocardial fibrosis at one month, assessed with LGE-CMR, after STEMI. Methods We included 65 patients with STEMI who underwent urgent revascularization with PCI in the first 12 hours from the onset of symptoms. The ISSTE was determined by summing the ST segment elevation in all registered ECG leads at presentation (ISSTE-1) and at 2 hours (ISSTE-2) after primary PCI. Blood samples were also collected at baseline and day-5 for determination of serum hs-CRP levels. At 1-month follow-up all patients under LGE-CMR (1.5T scanner) for evaluation of the myocardial scar extent (volume, percentage, transmurality). Results ISSTE-2 was significantly correlated with day-5 hs-CRP serum levels (r = 0.546, 95%CI: 0.030-0.832, p = 0.037), although no significant correlations were noted with baseline hs-CRP levels (r= 0.238, p = 0.407). There were no significant correlations between ISSTE-1 score and the myocardial scar percentage (r = 0.241, p = 0.11) or high transmurality volume (r = 0.194, p = 0.21), while ISSTE-2 significantly correlated with myocardial scar mass (r = 0.406, 95%CI: 0.107-0.637 p = 0.007) and high transmurality volume (r = 0.344, 95%CI: 0.0320-0.596, p = 0.0273). The restoration of the ST segment, reflected by the difference between ISSTE-1 and ISSTE -2 is correlated with the infarct size mass (r = 0.336, 95%CI: 0.0307 -0.584, p = 0.027). Conclusion The magnitude of ST segment elevation determined at 2 hours after PCI was associated with the inflammatory response at day 5 after STEMI and it may serve as a predictor for the extent of the myocardial scar tissue determined with LGE-CMR at 1 month following STEMI. The ISSTE-1 score calculated at presentation does not reflect extent of the affected myocardial tissue following PCI.

Tuberculous myocarditis presenting as a refractory ventricular tachycardia of biventricular origin

Ventricular tachycardia (VT) is one of the difficult clinical problems for the physician. Its evaluation and treatment are complicated because of its life-threatening nature and urgent need of rapid management. Any process that creates myocardial scar tissue could be the substrate for ventricular tachycardia. The coronary artery disease is the most common cause of myocardial scar. The dilated cardiomyopathies, hypertrophic cardiomyopathy, right ventricular dysplasia, Chagas disease, sarcoidosis, myocarditis including tubercular and other chronic granulomatous conditions and surgical incisions in the ventricle also can create myocardial scar and can lead to ventricular tachycardia. Occasionally, the arrhythmia may be well-tolerated, but in most of the situations it is associated with grave, life-threatening hemodynamic compromise. Regardless of the arrhythmia mechanism, the severity of clinical symptoms and hemodynamic compromise determines the urgency with which VT must be treated. Rarely, patients present with repetitive runs of nonsustained or sustained VT despite the medical treatment and poorly respond to the conventional treatment. Such refractory VT may cause a tachycardia-induced cardiomyopathy in long run. In such cases, long-term management also include looking beyond the VT and work up for the possible and treatable cause of VT. Here we are presenting a case report of a young patient with tubercular myocarditis who has presented to us with recurrent ventricular tachycardia of both right bundle and left bundle branch block morphology and LV dysfunction. A review of literature has been carried out on causes and management of refractory VT.Journal of College of Medical Sciences-Nepal, 2011, Vol-7, No-2, 60-66DOI: http://dx.doi.org/10.3126/jcmsn.v7i2.6686