Annie Trinh

Lower circulating Sta-Liatest D-Di levels in patients with aortic intramural hematoma compared with classical aortic dissection

Objective:To compare the diagnostic value of circulating Sta-Liatest D-Di levels in classic acute aortic dissection (AAD) and in aortic intramural hematoma (AIH), a variant of AAD without a patent false lumen. Design:Single-center retrospective case-control study. Setting:University Hospital of Strasbourg, France. Patients:Ninety-four consecutive patients with both confirmed AAD and d-dimer measurements at entry were included. d-dimer levels were assayed by the immunoturbidimetric method Sta-Liatest D-Di (Diagnostica Stago, Asnieres sur Seine, France). Intervention:Patient characteristics and clinical evolution were analyzed. Measurements and Main Results:Eighty-four patients (89%) presented a classic AAD with patent false lumen and ten (11%) presented an AIH. Clinical presentation did not differ between the two groups. The mortality rate was 0% in AIH and 26% in classic AAD. d-dimer levels were significantly lower in patients with AIH (median, 1230 ng/mL; interquartile range, 685–2645 ng/mL) than in patients with AAD with patent false lumen (median value, 9290 ng/mL; interquartile range, 3890–20,000 ng/mL; p = 0.008). All patients with AAD and patent false lumen had d-dimer levels above the threshold of 400 ng/mL (sensitivity 100%). However, one patient with AIH presented d-dimer levels below the threshold. Therefore, the sensitivity of the d-dimer test in detecting AIH was 90%. Conclusions:Sta-Liatest D-Di levels are lower in AIH than in AAD with patent false lumen. This test can quite possibly be negative in the case of intramural hematoma. This feature must be considered when interpreting d-dimer levels in patients with acute aortic syndrome.

Transient left ventricular dysfunction syndrome during anaphylactic shock: Vasospasm, Kounis syndrome or epinephrine-induced stunned myocardium?

Abstract Transient left ventricular dysfunction syndrome (TVLDS) has been rarely observed during anaphylactic shock and its pathophysiology remains still enigmatic. Multivessel epiicardial coronary spasm or coronary microvascular impairment were suggested as primary causative mechanism. Alternatively, the release of various inflammatory mediators including histamine could induce a coronary artery spasm or erosion/rupture of an atheromatous plaque contributing to TLVDS. Challenging this paradigm, a direct catecholamine acute toxicity was recently proposed as a causative mechanism of the stunned myocardium observed in TLVDS. We report a patient with severe TLVDS during anaphylactic shock. Whilst ECG depicted a drastic ST segment elevation in the anterior leads, cardiac catheterism confirms the co-existence of severe reduction of systemic vascular resistance and normal coronary angiogram. In the absence of any documented spasm or perfusion abnormalities, the defective uptake of 123 I-metaiodobenzyl-guanidine ( 123 I-mIBG) in the hypocontractile LV segments suggests that epinephrine-induced stunned myocardium is the main mechanism of LV systolic dysfunction. This report highlights that excess doses of epinephrine might contribute to TLVDS through direct myocardial stunning. The possible noxious contribution of other mediators such as histamine or cytokines released in the Kounis syndrome remains to be established.

Effects of Transcutaneous Aortic Valve Implantation on Aortic Valve Disease-Related Hemostatic Disorders Involving von Willebrand Factor

BACKGROUND Aortic valve stenosis (AVS) can be complicated by bleeding associated with acquired type 2A von Willebrand syndrome. The association of AVS and gastrointestinal bleeding from angiodysplasia is defined as Heyde syndrome. We sought to evaluate the effect of transcutaneous aortic valve implantation (TAVI) on hemostasis disorders and to assess its effectiveness to treat Heyde syndrome. METHODS We prospectively enrolled 49 consecutive patients with severe AVS addressed for TAVI at our institution. Biological hemostasis parameters involving von Willebrand factor (vWF) were assessed at baseline and 1 week after the procedure. RESULTS At baseline, a significant link between vWF abnormalities and the severity of AVS was evidenced: mean aortic transvalvular gradient was negatively correlated with the levels of vWF antigen (vWF:Ag) (r = -0.29; P < 0.05), vWF ristocetin cofactor activity (r = -0.402; P = 0.006), and vWF collagen-binding activity (vWF:CB; r = -0.441; P = 0.005). One week after the procedure, a significant increase of vWF:Ag, vWF ristocetin cofactor activity, and vWF:CB was evidenced in the whole cohort (respectively, 3.32 vs. 2.29 IU/mL, P < 0.001; 2.98 vs. 1.86 IU/mL, P < 0.001; and 3.16 vs. 2.16 IU/mL, P < 0.001). Patients with pre-TAVI vWF abnormalities consistent with a type 2A vWF syndrome (ratio vWF:CB/vWF:Ag < 0.7) preferentially improved their vWF function with respect to patients with a normal ratio (relative increase of vWF:CB of 63.8% vs. 3.5%). CONCLUSIONS Hemostasis parameters involving vWF are improved after TAVI, especially in patients with pre-existing abnormalities consistent with acquired type 2A von Willebrand syndrome.

Impact of Malignancies in the Early and Late Time Course of Takotsubo Cardiomyopathy

BACKGROUND Although the relationship between malignancies and catecholamine-induced myocardial stunning remains largely speculative, it has been suggested that the presence of cancer may lower the threshold for stress stimuli and/or may aggravate cardiac adrenoreceptor sensitivity. We sought to investigate whether associations exist between a previous or current diagnosis of malignancy, diagnostic parameters during hospitalization and death in takotsubo. METHODSANDRESULTS The 154 takotsubo patients were retrospectively identified between May 2008 and December 2014. Previous history of malignancy was identified in 44 patients (28.5%). Cardiac arrest was present at admission in 13 patients (8.4%). Intra-aortic balloon pump was inserted in 16 patients (10.4%). In patients with malignancy, higher B-type natriuretic peptide (BNP), leukocyte and C-reactive protein (CRP) peaks could be observed during the hospital phase. Initial impairment of left ventricular ejection fraction was negatively related to BNP, leukocyte, and CRP peaks. At a median follow-up of 364 days, all-cause death occurred in 41 patients (26.6%) and cardiac death in 12 patients (7.7%). Multivariate Cox regression analysis identified malignancy (hazard ratio 4.77 (1.02-22.17), leukocyte peak and age as independent predictors of cardiac death. Malignancy (2.62 (1.26-5.44), leukocyte peak (1.05 (1.01-1.08) and initial cardiac arrest (6.68 (2.47-18.01) were identified as independent predictors of overall mortality. CONCLUSIONS In the present takotsubo patients, the prevalence of malignancy was high and may have affected cardiovascular outcomes through the activation of inflammatory and neurohormonal mechanisms. (Circ J 2016; 80: 2192-2198).

Recurrent form of neurogenic stunned myocardium: Is myocardial adrenergic receptor distribution a dynamic process?

Neurogenic stunned myocardium mediated by stress-induced catecholamine acute release is considered as the central causative mechanism of transient left ventricular dysfunction syndrome (TVLDS). Interindividual differences in both LV β-adrenergic receptor density and sympathetic innervation were proposed to explain the atypical forms of TVLDS. Whether this distribution is independent of age or may vary during ageing still remains unclear. We report a recurrent form of TLVDS characterized by two different patterns. Whilst myocardial receptor distribution or sympathetic innervation appears to follow a dynamic process, the precise determinants of these variations remain largely unknown.

Takotsubo and Takotsubo-like syndrome: A common neurogenic myocardial stunning pathway?

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CT-ADP Point-of-Care Assay Predicts 30-Day Paravalvular Aortic Regurgitation and Bleeding Events following Transcatheter Aortic Valve Replacement

BACKGROUND Paravalvular aortic regurgitation (PVAR) remains a frequent postprocedural concern following transcatheter aortic valve replacement (TAVR). Persistence of flow turbulence results in the cleavage of high-molecular-weight von Willebrand multimers, primary haemostasis dysfunction and may favour bleedings. Recent data have emphasized the value of a point-of-care measure of von Willebrand factor-dependent platelet function (closure time [CT] adenosine diphosphate [ADP]) in the monitoring of immediate PVAR. This study examined whether CT-ADP could detect PVAR at 30 days and bleeding complications following TAVR. METHODS CT-ADP was assessed at baseline and the day after the procedure. At 30 days, significant PVAR was defined as a circumferential extent of regurgitation more than 10% by transthoracic echocardiography. Events at follow-up were assessed according to the Valve Academic Research Consortium-2 consensus classification. RESULTS Significant PVAR was diagnosed in 44 out of 219 patients (20.1%). Important reduction of CT-ADP could be found in patients without PVAR, contrasting with the lack of CT-ADP improvement in significant PVAR patients. By multivariate analysis, CT-ADP > 180 seconds (hazard ratio [HR]: 5.1, 95% confidence interval [CI]: 2.5-10.6; p < 0.001) and a self-expandable valve were the sole independent predictors of 30-day PVAR. At follow-up, postprocedural CT-ADP >180 seconds was identified as an independent predictor of major/life-threatening bleeding (HR: 1.7, 95% CI [1.0-3.1]; p = 0.049). Major/life-threatening bleedings were at their highest levels in patients with postprocedural CT-ADP > 180 seconds (35.2 vs. 18.8%; p = 0.013). CONCLUSION Postprocedural CT-ADP > 180 seconds is an independent predictor of significant PVAR 30 days after TAVR and may independently contribute to major/life-threatening bleedings.

Atrial arrhythmias in Takotsubo cardiomyopathy: incidence, predictive factors, and prognosis

Aims Takotsubo cardiomyopathy (TTC) is a stress-related transient cardiomyopathy. It is unclear whether TTC is associated with poorer prognosis when atrial arrhythmia (AA), atrial fibrillation or flutter, occurs. The purpose of this study was to assess the incidence of AA in patients with TTC, predictive factors of AA, and its association with mortality. Methods and results We studied 214 consecutive cases of TTC over 8 years. The study cohort was divided into two groups-those with newly diagnosed AA (AA-group) and those without (non-AA group). AA occurred in 24.8% of the patients. The AA group presented with lower left ventricular ejection fraction (LVEF) on admission and higher cardiac arrest rate. Admission and peak levels of troponin, B-type natriuretic peptide (BNP), C-reactive protein (CRP), and leucocytes were higher in the AA group. In-hospital, 30-day, cardiovascular, and all-cause mortality were significantly higher in the AA group. Independent predictors of newly diagnosed AA were troponin peak [odds ratio (OR) 1.03 (1.003-1.06); P = 0.029], CRP peak [OR 1.006 (1.001-1.01); P = 0.026], and LVEF on admission [OR 0.96 (0.93-0.99); P = 0.01]. Newly diagnosed AA was not predictive of mortality. The BNP peak [OR 1.00 (1.000-1.001); P = 0.022] and leucocytes peak [OR 1.095 (1.034-1.16); P = 0.002] were predictive factors of in-hospital mortality. LVEF upon discharge [OR 0.935 (0.899-0.972); P = 0.001] and leucocytes peak [OR 1.068 (1.000-1.139); P = 0.049] were predictive of cardiovascular death. Conclusion Newly diagnosed AA is frequently observed in patients presenting with TTC and is associated with poorer short- and long-term prognosis. Inflammation, myocardial damage, and LVEF are predictors of AA onset and cardiovascular mortality.

0353: Impact of TAVI on primary hemostasis, von Willebrand factor and Heyde’s syndrome: a prospective monocenter study

Background Aortic valve stenosis (AVS) can be complicated by bleeding associated with acquired type 2A von Willebrand syndrome. The association of AVS and gastrointestinal bleeding from angiodysplasia is defined as Heyde’s syndrome. We sought to evaluate the impact of TAVI on primary hemostasis disorders and to assess its effectiveness to treat Heyde’s syndrome. Methods We prospectively enrolled 49 consecutive patients with severe AVS referred to our institution for TAVI. Biological primary hemostasis parameters were assessed at baseline and one week after the procedure. Results At baseline, a significant link between vWF abnormalities and the severity of AVS was evidenced: mean aortic transvalvular gradient was negatively correlated with the levels of vWF antigen (vWF: Ag) (r=–0.29, p Conclusion Primary hemostasis parameters involving vWF are improved after TAVI, especially in patients with preexisting abnormalities consistent with acquired type 2A von Willebrand syndrome. Moreover, our observations, although limited to a small single-center study, suggest that Heyde’s syndrome can be cured by TAVI.

TCT-765 Impact Of TAVI On Primary Hemostasis, Von Willebrand Factor And Heyde’s Syndrome: A Prospective Monocenter Study

Aortic valve stenosis (AVS) can be complicated by bleeding associated with acquired type 2A von Willebrand syndrome. The association of AVS and gastrointestinal bleeding from angiodysplasia is defined as Heydes syndrome. We sought to evaluate the impact of TAVI on primary hemostasis disorders and