Sylvain Grall

CMR assessment after a transapical-transcatheter aortic valve implantation

AIMS To describe the time course of myocardial scarring after transapical-transcatheter aortic valve implantation (TA-TAVI) with the Edwards SAPIEN XT™ and the Edwards SAPIEN™ prosthesis in a 3-month follow-up study using cardiac magnetic resonance imaging (CMR). METHODS In 20 TA-TAVI patients, CMR was performed at discharge and 3 months (3M). Cine-MRI was used for left ventricular (LV) functional assessment, and late gadolinium enhancement (LGE) imaging was employed for detecting the presence of myocardial scarring. Special attention was given to any artifacts caused by the prosthesis, which were consequently defined using a three-grade artifact scale. RESULTS We systematically reported the presence of small LGE hyperintensity relating to the apical segment, with no variation found between discharge and 3M (2.8±1.6g vs. 2.35±1.1g). LV ejection fraction, end-diastolic, and end-systolic volumes did not significantly vary. A small area of apical akinesia was observed, with no improvement at follow-up. Whereas the Edwards SAPIEN XT™ prosthesis and the Edwards SAPIEN™ prosthesis are both constituted by metallic stenting structure, the Edwards SAPIEN™ was responsible for a larger signal void, thus potentially limiting the diagnostic performance of CMR. CONCLUSIONS CMR may be performed safely in the context of TA-TAVI. The presence of a very small apical infarction correlating with focal akinesia was observed. As expected, the Edwards SAPIEN XT™ prosthesis was shown to be particularly suitable for CMR assessment.

ECG characteristics according to the presence of late gadolinium enhancement on cardiac MRI in hypertrophic cardiomyopathy

Background Late gadolinium enhancement (LGE) on cardiac MRI (CMR) has been described as an independent predictive factor of cardiovascular events among patients with hypertrophic cardiomyopathy (HCM). LGE and Q waves are considered as myocardial scar markers but their relation in the context of HCM is poorly established and has to be more supported. The objective of the study was to compare ECG findings in the presence or absence of LGE. Methods 42 patients with HCM confirmed by CMR were included in the study. ECG abnormalities including abnormal Q waves and five ECG scores of left ventricular hypertrophy were assessed and compared according to LGE presence and its extension. Some CMR features, such as septal to posterior wall thickness ratio, were also studied according to the presence of LGE and the presence of abnormal Q waves. Results Abnormal Q waves were more prevalent in the LGE (+) group (60% vs 12%; p=0.002), but there was no correlation between location of Q waves on ECG and territory of LGE on CMR. Among patients with LGE, quantitative analysis of LGE was not different in the presence or absence of Q waves. In contrast to the LGE mass, septal to posterior wall thickness was higher in patients with abnormal Q waves (2.3±0.7 vs 1.6±0.5; p=0.012). Conclusions Although abnormal Q waves were more prevalent in the presence of LGE, no correlation was found with the LGE location and extent. These data suggest that abnormal electrical activation of the hypertrophied ventricular septum represented by a high septal to posterior wall thickness ratio seems to be an important mechanism of abnormal Q waves in HCM.

Reverse iatrogenic Takotsubo syndrome after accidental bolus of norepinephrine in the setting of sepsis.

A 17-year-old male was referred to the resuscitation department for sepsis related to choleriform diarrhoea. The physical examination revealed a tachycardia with a heart rate of 110 bpm and low blood pressure 80/40 mm Hg. No signs of heart failure were noticed and no abnormality was observed in the first electrocardiogram. Laboratory tests showed an important inflammatory syndrome with procalcitonin of 194 ng/mL. B-type natriuretic peptide (BNP) and troponin levels were 176 pg/mL and 0.52 μg/L, respectively. Transthoracic echocardiogram revealed preserved left ventricular systolic function (left ventricular ejection fraction [LVEF] about 70%) with a normal wall motion. Vascular filling and continuous norepinephrine infusion were indicated. However, the patient accidently received a bolus of 2 mg of norepinephrine. Immediately after, he reported chest pain with dyspnoea; crackles were auscultated. The second electrocardiogram revealed a depression of the ST segment in apico-lateral leads (Fig. 1). A comparative echocardiogram showed an impairment of LVEF (40%) with global hypokinesia and apical ballooning (Fig. 2A). Both BNP and troponin levels increased to 1500 pg/mL and 2.33 μg/mL, respectively. Norepinephrine was interrupted and replaced by dobutamine infusion. The patient required non invasive ventilation for 48 h; thereafter, the outcome was good with improvement of symptoms and haemodynamic status. A control echocardiogram confirmed the recovery of left ventricular function (LVEF 55%) and the absence of dilation (Fig. 2B). Multiple blood cultures were negative, and no toxin was detected in blood and urine analyses. A cardiac resonance imaging performed seven days later showed a preserved LVEF with no late enhancement (Fig. 3). Takotsubo syndrome (TSS) is characterised by transient wall motion abnormalities commonly involving the apical segment. Cases of iatrogenic TSS occurring after high-dose epinephrine administration have been reported, particularly in the setting of anaphylaxia, confirming the hypothesis that the underlying aetiology is related to excessive catecholamine endogenous or exogenous release. To the best of our knowledge, this is the first case reported in the setting of sepsis. The outcome is generally good with spontaneous resolution particularly in patients with no comorbidities; however, haemodynamic support might be necessary in some cases until the recovery of left ventricular systolic function. Figure 1. Electrocardiogram immediately after accidental norepinephrine bolus Figure 2. Comparative echocardiograms immediately after accidental norepinephrine bolus (A) and 48 h later (B)

047: Gender difference in mortality after ST-segment elevation myocardial infarction in the Registre d’Infarctus Maine-Anjou (RIMA)

Background A greater mortality in women versus men in ST-segment elevation myocardial infarction (STEMI) is now well documented but remains unexplained. Methods We compared outcomes for STEMI in the “Registre d’Infarctus Maine-Anjou” (RIMA) from 2003 to 2009 between men and women. Results We analyzed data from 390 women (29%) and 962 men (71%) admitted for STEMI. Women were older, 72.93±14.21 versus 61.70±14.14 years old (p Conclusion Our study suggests that older age in women explains most of the mortality difference.