Psychosocial and physical long-term outcome in patients with a history of takotsubo cardiomyopathy or myocardial infarction - a multi-centered case control study.

Physical long-term impacts of Takotsubo Cardiomyopathy (TTC) remain controversial and an underestimation of their severity becomes increasingly evident. Even less is known about mental long-term impacts of TTC. This study aims at a better understanding of the physical and mental long-term effects of TTC in comparison to myocardial infarctions (MI). On average 5 years after disease onset, 68 TTC patients and 68 age- and sex-matched MI patients were assessed for disease-related quality of life, depression, anxiety, chronic stress, social support, resilience, and life events prior to disease onset. Scores of TTC and MI patients were compared to each other and to normative references values. Regression analyses were used to evaluate the predictive value of the number of life events prior to disease onset for physical and mental long-term outcomes. Both groups displayed higher scores in depression and anxiety, higher levels of chronic stress, and lower scores in physical and mental quality of life in comparison to norm samples, while social support did not differ from norms. No differences between the two patient groups were observed. Within both groups, the majority of patients (TTC: 69.1%; MI: 60.3%) reported stressful life events prior to disease onset. In TTCs and MIs, the number of events had a significant impact on long-term mental health and chronic stress. Notably, both patient collectives scored higher in resilience than healthy controls. Results suggest negative long-term impacts of TTC on mental and physical wellbeing, comparable to those of MI. Besides a good somatic-medical care, psychotherapeutic support, including the development of functional coping strategies, might be warranted for TTC patients. The long-term impact of TTC should be taken as serious as that of MI.

[Patient care in the acute phase of stress induced cardiomyopathy (Tako-Tsubo cardiomyopathy)--and thereafter?]. / Patientenversorgung in der akuten Phase der stressinduzierten Kardiomyopathie (Tako-Tsubo-Kardiomyopathie)--und danach?

The prognosis of patients presenting with Tako-Tsubo cardiomyopathy (TTC) is generally considered to be favorable. However, in the acute phase of the disorder complications are not infrequent and, therefore, continuous monitoring and consistent therapy in an intensive care unit is essential. Typical complications in patients with TTC are cardiogenic shock, obstruction of the left ventricular outflow tract (LVOT), occasionally accompanied by acute mitral regurgitation, arrhythmias, predominantly torsade de pointes tachycardias due to QT prolongation, left ventricular (LV) thrombus formation with or without consecutive thromboembolic events, and LV rupture. After confirmation of TTC by coronary angiography, repeat echocardiography should be performed. A standardized therapy for patients with TTC has so far not been established. Recommendations for the acute phase include the administration of anxiolytic agents for patients who present with preceding emotional stress, consistent therapy of physical stressors (such as pain or asthma) and avoidance of catecholamine therapy. Shock due to LVOT obstruction is treated by administration of volume and ß-blockers. With respect to the occurrence of torsade de pointes tachycardias, drugs which might cause QT prolongation should not be given. The notable incidence of LV thrombus formation justifies therapeutic anticoagulation. Systematic studies and treatment recommendations for the prophylaxis of recurrent TTC do not exist. The recently reported association between TTC and malignant disorders should prompt tumor screening and subsequent preventive medical checkups in patients affected by TTC.

Adenosine inhibits norepinephrine release in the postischemic rat heart: the mechanism of neuronal stunning.

OBJECTIVE: Numerous studies support the concept of impaired postischemic sympathetic neurotransmission in the heart. We hypothesized that postischemic neuronal dysfunction (neuronal stunning) is caused by a transient suppression of exocytotic norepinephrine (NE) release from sympathetic nerve terminals. Furthermore, we assessed the role of presynaptic adenosine-receptors and alpha2-adrenoceptors in neuronal stunning. METHODS AND RESULTS: Exocytotic NE release was induced by two electrical field stimulations (S(1) and S(2)) in isolated perfused rat hearts. S(1) was performed under baseline conditions and S(2) either during or following intervention. Results are expressed as mean S(2)/S(1) ratios+/-S.E.M. Stepwise increase of global ischemic periods (10, 20, and 30 min) induced a progressive suppression of NE release in the postischemic hearts, which was reversible during reperfusion. Both the degree and duration of NE suppression was dependent on the extent of the preceding ischemic period. Following 10-min ischemia complete recovery of NE release was achieved after 5-min reperfusion (1.07+/-0.12), whereas 5-min reperfusion did not restore NE release after 30 min (0.36+/-0.07) of ischemia. The adenosine-receptor antagonists 8-phenyltheophylline (8-PT; non-selective) and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; adenosine A1-receptor subtype selective) significantly increased NE release after 30-min ischemia and 5-min reperfusion (0.78+/-0.06 and 0.64+/-0.07), while in the same experimental protocol blockade of alpha2-adrenoceptors by yohimbine failed to restore the postischemic release (0.24+/-0.06). In non-ischemic hearts the adenosine analogue R(-)N(6)-(2-phenylisopropyl)adenosine (R-PIA) resulted in a marked suppression of NE release (0.61+/-0.07). The inhibitory effect of R-PIA and 2-chloro-N(6)-cyclopentyladenosine (CCPA; adenosine A1-receptor subtype selective agonist) persisted 5 min after cessation of R-PIA (0.62+/-0.05) and CCPA (0.58+/-0.04). Activation of alpha2-adrenoceptors by 5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine (UK 14,304) also caused a reduction of NE release (0.50+/-0.02), but the release increased to control levels 5 min after cessation of UK 14,304 (0.90+/-0.06). CONCLUSIONS: The results establish the phenomenon of neuronal stunning in terms of a postischemic suppression of exocytotic NE release and provide evidence that neuronal stunning is mediated by endogenous adenosine through activation of presynaptic adenosine A1-receptors.

Norepinephrine release is reduced in cardiac tissue of Type 2 diabetic patients.

AIMS/HYPOTHESIS: The aim of this study was to assess whether cardiac catecholamine release is affected in patients with Type 2 diabetes mellitus. METHODS: A trial tissue was obtained from 19 diabetic (Type 2) and 43 non-diabetic patients undergoing coronary surgery. Endogenous norepinephrine release was examined under baseline conditions as well as during electrical field stimulation (effective voltage 5 V, stimulation frequency 4 Hz, pulse width 2 msec) by high performance liquid chromatography and electrochemical detection. Cardiac function and arterial blood pressure was assessed from coronary angiography. RESULTS: In atrial tissue from diabetic patients, stimulation-induced norepinephrine release was reduced by 25% compared with non-diabetic patients, while baseline norepinephrine release did not differ between both groups. Preoperative plasma glucose and haemoglobin A(1C) concentrations were increased in patients with diabetes, however, no relation was found to catecholamine release. Diabetic and non-diabetic patients did not differ regarding left ventricular ejection fraction and arterial blood pressure. CONCLUSION/INTERPRETATION: Cardiac norepinephrine release is suppressed in patients with Type 2 diabetes which could contribute to sympathetic neuropathy. The difference of norepinephrine release in diabetic and non-diabetic patients was independent of cardiac function and arterial blood pressure.