Abstract

Q waves and negative T waves are common electrocardiographic (ECG) abnormalities in patients with Hypertrophic Cardiomyopathy (HCM). Several studies correlated ECG findings with presence and extent of fibrosis and hypertrophy, however, their significance remains incompletely clarified. Our study aimed to explain the mechanism behind Q and negative T waves by comparing their positions on a 12-lead ECG with phenotypes observed at Late Gadolinium Enhancement (LGE) Cardiac Magnetic Resonance (CMR). 12-lead ECG and LGE-CMR were performed in 88 consecutive patients with HCM (42 SD 16 years, 65 males). Using Delta Thickness ratio (DT ratio), and “global” and “parietal” LGE at CMR, the extent and distribution of myocardial hypertrophy and fibrosis were studied in correlation with ECG abnormalities. Q waves in different leads were not associated with “parietal” LGE score. Lateral Q waves correlated with an increased DT ratio Inferior Septum/Lateral wall (p = 0.01). A similar correlation between inferior Q waves and an increased DT Ratio Anterior wall/Inferior wall was of borderline statistical significance (p = 0.06). As expected, ECG signs of LV hypertrophy related to a raised Left Ventricular Mass Index (LVMI) (p < 0.0001) and mean wall thickness (p = 0.01). Depolarization disturbances, including negative T waves in lateral (p = 0.044) and anterior (p = 0.031) leads correlated with “parietal” LGE scores while QT dispersion (p = 0.0001) was associated with “global” LGE score. In HCM patients, Q waves are generated by asymmetric hypertrophy rather than by myocardial fibrosis, while negative T waves result from local LGE distribution at CMR.

Abstract

Late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) has been recommended to distinguish Tako-tsubo cardiomyopathy (TTC) from either acute myocardial infarction or myocarditis. 44 consecutive patients with confirmed Mayo Clinic criteria for TTC underwent CMR imaging at 1.5 Tesla during the acute phase. 10 patients who had CMRI to exclude scar related ventricular tachycardia, and had negative studies, were used as negative controls. LGE was quantitated at two signal intensity thresholds (CircleCVi software) at > 2 and > 5 standard-deviations (SD) above reference myocardium, and compared to biomarkers. Mean door-to-CMR time was 57 hours. 18 patients (41%) had LGE > 2 SD localized to the area of abnormal wall motion, representing 28.9 ± 11.2% LV mass. In 16 of these 18 patients (89%) LGE signal intensity was > 5 SD above normal myocardium, representing 12.1 ± 10% LV mass. LGE signal intensity was significantly greater in TTC than in matched controls (p < 0.05) but lower than in STEMI patients (p < 0.05). Mean troponin was significantly higher in LGE positive patients (2.5 ± 1.8 vs 4.4 ± 6.9, p = 0.001). Mean ejection fraction (EF) by CMR was 45% ± 8.7 in LGE-negative, and 40% ± 7.1 in LGE-positive patients (p = 0.37). Recovery of segmental function was confirmed at follow-up, mean EF was 59% in both groups. LGE was present in 41% of cases of TTC, 89% of which had intense enhancement > 5 SD above normal myocardium. Presence of LGE was associated with worse myocardial injury in the acute setting, with no difference in recovery of function.

Abstract

Transthoracic Doppler-echocardiography (TTE) can estimate mean pulmonary arterial pressure (MPAP) and pulmonary capillary wedge pressure (PCWP) reliably, and cardiac magnetic resonance (CMR) is the best modality for non-invasive measurement of cardiac output (CO). We speculated that the combined use of TTE and CMR could provide a feasible method for non-invasive measurement of pulmonary vascular resistance (PVR) in pulmonary arterial hypertension (PAH). Right heart catheterization (RHC) was undertaken in 77 patients (17M/60F) with PAH, and simultaneous TTE was carried out to evaluate MPAP, PCWP and CO. Within 2 days, CO was measured again with CMR in similar physiological status. Then, PVR was calculated with the integrated non-invasive method: TTE-derived (MPAP–PCWP)/CMR-derived CO and the isolated TTE method: TTE-derived (MPAP–PCWP)/TTE-derived CO, respectively. The PVR calculated with integrated non-invasive method correlated well with RHC-calculated PVR (r = 0.931, 95% confidence interval 0.893 to 0.956). Between the integrated non-invasive PVR and RHC-calculated PVR, the Bland–Altman analysis showed the satisfactory limits of agreement (mean value: − 0.89 ± 2.59). In comparison, the limits of agreement were less satisfactory between TTE-calculated PVR and RHC-calculated PVR (mean value: − 1.80 ± 3.33). Furthermore, there were excellent intra- and inter-observer correlations for the measurements of TTE and CMR (P < 0.001 for all). The combined use of TTE and CMR provides a clinically reliable method to determine PVR non-invasively. In comparison with RHC, the integrated method shows good accuracy and repeatability, which suggests the potential for the evaluation and serial follow-up in patients with PAH. In PAH, the non-invasive measurement of PVR is very important in clinical practice. Up to now, however, the widely accepted non-invasive method is still unavailable. Since TTE can estimate (MPAP–PCWP) reliably and CMR is the best image modality for the measurement of CO, the combined use of two modalities has the potential to determine PVR non-invasively. In this research, the integrated non-invasive method showed good diagnostic accuracy and repeatability compared with RHC. Therefore, it might be a feasible method for non-invasive measurement of PVR in patients with PAH.