Brachial Artery Flow-mediated Dilation in Patients with Tako-Tsubo Cardiomyopathy

Vasilieva, Elena; Vorobyeva, I.; Lebedeva, A.; Urazovskaya, Irina L.; Kalinskaya, Anna; Скрыпник, Д. В.; Shpektor, A.

doi:10.1016/j.amjmed.2011.05.033

Cited by 24 publications

(14 citation statements)

References 15 publications

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“…Moreover, endothelial injury is correlated with increased levels of catecholamines 10. During the acute phase of TTS, a systemic inflammation11 and severe endothelial dysfunction can be found 12, 13. Finally, a hypercoagulable state induced by a catecholamine surge may also be present 14.…”

Section: Discussionmentioning

confidence: 99%

“…Angiotensin‐converting enzyme inhibitors or angiotensin II receptor blockers could have some benefit in term of improved survival at 1 year 3. β‐Blockers showed no effect on survival and recurrence rate,3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38 whereas calcium antagonists could be used if coronary vasospasm has been proven during coronary angiogram or with acetylcholine test 32…”

Section: Discussionmentioning

confidence: 99%

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Left Ventricular Thrombi in Takotsubo Syndrome: Incidence, Predictors, and Management: Results From the GEIST (German Italian Stress Cardiomyopathy) Registry

Santoro

Stiermaier

Tarantino

et al. 2017

JAHA

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BackgroundLeft ventricular (LV) thrombi during Takotsubo syndrome represent a potential complication and can be associated with cerebrovascular embolic events. The aim of this study was to evaluate the exact incidence, predictors, and management strategies of LV thrombi in patients with Takotsubo syndrome.Methods and ResultsWe enrolled 541 consecutive patients in a multicenter international registry. Clinical features and echocardiographic data at admission, during hospitalization, and after 3 months were evaluated. Survival rates for long‐term follow‐up (mean 984±908 days) were recorded. Twelve Takotsubo syndrome patients (2.2%) developed LV thrombi (all female presenting with apical ballooning pattern). All patients with LV thrombi were treated with oral anticoagulation therapy; however, 2 (17%) had a stroke before treatment initiation. These patients were characterized by a higher prevalence of ST‐elevation (56% versus 16%; P<0.001) and higher troponin I levels (10.8±18.3 ng/mL versus 3.5±4.3 ng/mL; P=0.001) as compared with those without LV thrombi. At multivariate analysis including age, sex, LV ejection fraction, ST‐elevation at admission, and apical ballooning pattern, troponin I level >10 ng/mL was the only predictor for LV thrombosis (hazard ratio 6.6, confidence interval, 1.01–40.0; P=0.04). After 3 months all LV thrombi disappeared. Oral anticoagulation therapy was interrupted in all patients except 1. At long‐term follow‐up, the survival rate was not different between patients with and without LV thrombi (84% versus 85%; P=0.99).Conclusions LV thrombi have a relatively low incidence among patients with Takotsubo syndrome and were detected in female patients with apical ballooning pattern and increased troponin levels. Oral anticoagulation therapy for 3 months seems reasonable in these high‐risk patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Left Ventricular Thrombi in Takotsubo Syndrome: Incidence, Predictors, and Management: Results From the GEIST (German Italian Stress Cardiomyopathy) Registry

Santoro

Stiermaier

Tarantino

et al. 2017

JAHA

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“…Complement activation can trigger endothelial adhesion molecule expression, and subsequent leukocyte rolling, arrest, and diapedesis. It is notable that there are several small studies indicating that patients with SCM have greater endothelial dysfunction than those with AMI even in the subacute phase ( 28 – 30 ). This dysfunction could be due to low-level complement activation, increased leukocyte adhesion, and release of reactive oxygen species.…”

Section: Discussionmentioning

confidence: 99%

Activation of Inflammatory and Pro-Thrombotic Pathways in Acute Stress Cardiomyopathy

Fitzgibbons

Edwards

Shaw

et al. 2017

Front. Cardiovasc. Med.

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Stress cardiomyopathy (SCM) is a unique cardiac disorder that more often occurs in women. SCM presents in a similar fashion as acute myocardial infarction (AMI), with chest pain, ECG changes, and congestive heart failure. The primary distinguishing feature is the absence of thrombotic coronary occlusion in SCM. How this reduction in cardiac function occurs in the absence of coronary occlusion remains unknown. Therefore, we tested the hypothesis that a targeted proteomic comparison of patients with acute SCM and AMI might identify relevant mechanistic differences. Blood was drawn in normal controls (n = 6), women with AMI (n = 12), or women with acute SCM (n = 15). Two-week follow-up samples were available in AMI (n = 4) and SCM patients (n = 11). Relative concentrations of 1,310 serum proteins were measured in each of the 48 samples using the SOMAscan assay. Women with AMI had greater myocyte necrosis, as reflected by a higher peak troponin I concentration (AMI 32.03 ± 29.46 vs. SCM 2.68 ± 2.6 ng/ml, p < 0.05). AMI and SCM patients had equivalent reductions in left ventricular ejection fraction [LVEF (%) 39 ± 12 vs. 37 ± 12, p = 0.479]. In follow-up, women with SCM had a greater improvement in cardiac function [LVEF (%) 60 ± 7 vs. 45 ± 13, p < 0.001]. No differentially expressed proteins were detected (absolute log2-fold change >1; q < 0.05) between AMI and SCM in the acute or recovery phase. However, when we compared normal controls to patients with AMI, there was differential expression of 35 proteins. When we compared normal controls to patients with SCM, 45 proteins were differentially expressed. In comparison to normal controls, biological processes such as complement, coagulation, and inflammation were activated in both AMI and SCM. There were four proteins that showed a non-significant trend to be increased in acute SCM vs. AMI (netrin-1, follistatin-like 3, kallikrein 7, kynureninase). Despite a lesser degree of myocardial necrosis than AMI, SCM is characterized by a similar activation of inflammatory, complement, and coagulation pathways. These findings may explain reported thromboembolic complications in the short term and elevated risk of mortality in the long term of SCM.

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“…Endothelial dysfunction, which constitutes the first step of atherosclerosis, has been suggested to be present in TTC [18], and the absence of relevant coronary narrowing is not synonymous of an atherosclerotic-free artery as different atherosclerotic lesions (e.g. macrophage infiltration, foam cells, fatty streak, intermediate lesions, and positive remodeling atheroma) might be present before the angiographic evidence of at least 50% coronary artery stenosis.…”

Section: Discussionmentioning

confidence: 99%

Tako-tsubo cardiomyopathy and coronary artery disease

Parodi

Citro²,

Bellandi³

et al. 2013

Coronary Artery Disease

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The presence of CAD is a rather common finding in a large proportion of patients with TTC. Thus, when the stenotic artery does not supply the dysfunctional myocardium or when the extent of dysfunctional myocardium is wider than the territory of distribution supplied by a single stenotic coronary artery, the presence of angiographically relevant CAD should not be considered an exclusion criterion for TTC.

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Brachial Artery Flow-mediated Dilation in Patients with Tako-Tsubo Cardiomyopathy

Cited by 24 publications

References 15 publications

Left Ventricular Thrombi in Takotsubo Syndrome: Incidence, Predictors, and Management: Results From the GEIST (German Italian Stress Cardiomyopathy) Registry

Left Ventricular Thrombi in Takotsubo Syndrome: Incidence, Predictors, and Management: Results From the GEIST (German Italian Stress Cardiomyopathy) Registry

Activation of Inflammatory and Pro-Thrombotic Pathways in Acute Stress Cardiomyopathy

Tako-tsubo cardiomyopathy and coronary artery disease

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