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      Recurrence of Stress-Induced (Takotsubo) Cardiomyopathy


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          Takotsubo cardiomyopathy is a recently recognized form of transient left ventricular dysfunction that is presumably precipitated by stress and may clinically resemble an acute coronary syndrome. These patients have an akinetic left ventricular apex in an unusual shape that resembles a takotsubo. Although reports of single episodes of takotsubo cardiomyopathy are not infrequent in recent medical literature, we report a case of recurrence that may provide more insight into the nature of this syndrome.

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          Most cited references 11

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          Adrenergic effects on the biology of the adult mammalian cardiocyte.

          To delineate the mechanism(s) of catecholamine-mediated cardiac toxicity, we exposed cultures of adult cardiac muscle cells, or cardiocytes, to a broad range of norepinephrine concentrations. Norepinephrine stimulation resulted in a concentration-dependent decrease in cardiocyte viability, as demonstrated by a significant decrease in viable rod-shaped cells and a significant release of creatine kinase from cells in norepinephrine-treated cultures. Norepinephrine-mediated cell toxicity was attenuated significantly by beta-adrenoceptor blockade and mimicked by selective stimulation of the beta-adrenoceptor, whereas the effects mediated by the alpha-adrenoceptor were relatively less apparent. When norepinephrine stimulation was examined in terms of cardiocyte anabolic activity, there was a concentration-dependent decrease in the incorporation of [3H]phenylalanine and [3H]uridine into cytoplasmic protein and nuclear RNA, respectively. The decrease in cytoplasmic labeling was largely attenuated by beta-adrenoceptor blockade and mimicked by selective stimulation of the beta-adrenoceptor, but alpha-adrenoceptor stimulation resulted in relatively minor decreases in cytoplasmic labeling. The norepinephrine-induced toxic effect appeared to be the result of cyclic AMP-mediated calcium overload of the cell, as suggested by studies in which pharmacological strategies that increased intracellular cyclic AMP led to decreased cell viability, as well as studies that showed that influx of extracellular calcium through the verapamil-sensitive calcium channel was necessary for the induction of cell lethality. Additional time-course studies showed that norepinephrine caused a rapid, fourfold increase in intracellular cyclic AMP, followed by a 3.2-fold increase in intracellular calcium [( Ca2+]i). These results constitute the initial demonstration at the cellular level that adrenergic stimulation leads to cyclic AMP-mediated calcium overload of the cell, with a resultant decrease in synthetic activity and/or viability.
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            Left ventricular apical ballooning due to severe physical stress in patients admitted to the medical ICU.

            We sought to assess the frequency and clinical implications of left ventricular apical ballooning (LVAB) in patients who had been admitted to the medical ICU for noncardiac physical illnesses. Ninety-two consecutive patients who were admitted to the medical ICU from March to May 2003 were prospectively enrolled. Patients underwent echocardiography on the day of ICU admission, and on the third and seventh days in the hospital. LVAB was defined as symmetric severe hypokinesia or akinesia of the left ventricular wall, except for the basal part of the left ventricle, with a < 50% ejection fraction. Of the 92 patients, 65 (71%) were men, and they had a mean (+/- SD) age of 63 +/- 11 years. LVAB was observed in 26 patients (28%), with a mean lowest ejection fraction of 33 +/- 8% (range, 19 to 46%). Compared with the 66 patients (72%) without LVAB, those with LVAB had a higher frequency of sepsis (62% vs 14%, respectively; p < 0.001), a higher prevalence of hypotension on ICU admission, more frequent use of inotropic agents, and a higher frequency of cardiomegaly and pulmonary edema (p < 0.005 for each). Sepsis was the only variable associated with the development of LVAB (odds ratio, 9.2; 95% confidence interval, 2.4 to 35.8; p < 0.001). The development of Q-wave or ST-segment displacement was associated with LVAB, but the sensitivities were 12% and 19%, respectively. Serum creatine kinase level was elevated in 12 of 26 patients (46%) with LVAB. The normalization of this condition occurred in 20 of 26 patients (77%) a mean duration of 7.4 +/- 5.6 days later (range, 2 to 25 days). The mean 2-month survival rate was lower in patients with LVAB than in those without (71 +/- 6% vs 52 +/- 10%, respectively; p = 0.047). LVAB develops in a considerable number of patients who are admitted to the medical ICU, and echocardiography is useful in detecting this phenomenon.
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              Assessment of Takotsubo (ampulla) cardiomyopathy using 99mTc-tetrofosmin myocardial SPECT--comparison with acute coronary syndrome.

              We assessed Takotsubo (ampulla) cardiomyopathy compared with acute coronary syndrome (ACS) using two-dimensional echocardiography and 99mTc-tetrofosmin myocardial SPECT. We examined 10 patients with Takotsubo cardiomyopathy and 16 with ACS at the time of emergency admission (acute phase), at three to nine days after the attack (subacute phase) and at one month after the attack (chronic phase). The left ventricle was divided into nine regions on echocardiograms and SPECT images, and the degree of abnormalities in each region was scored in five grades from normal (0) to severely abnormal (4). Coronary angiography revealed total or subtotal occlusion in patients with ACS but no stenotic legions in those with Takotsubo cardiomyopathy. The amount of ST segment elevation (mm) was 7.9 +/- 3.4 in patients with Takotsubo cardiomyopathy and 7.3 +/- 3.7 in those with ACS (N.S.). Abnormal wall motion scores on echocardiograms were 13.8 +/- 4.4, 4.4 +/- 3.8 and 1.8 +/- 2.3 during the acute, subacute and chronic phases in patients with Takotsubo cardiomyopathy, and 13.9 +/- 4.0, 11.7 +/- 3.7, 7.6 +/- 4.2, respectively in patients with ACS. The value of MB fraction of creatine phosphokinase (IU/l) was 34 +/- 23 in patients with Takotsubo cardiomyopathy and 326 +/- 98 in those with ACS (p < 0.001). Abnormal myocardial perfusion scores on 99mTc-tetrofosmin myocardial SPECT were 11.4 +/- 3.2, 3.2 +/- 3.3 and 0.7 +/- 1.1 during the acute, subacute and chronic phases respectively, in patients with Takotsubo cardiomyopathy, and 15.8 +/- 4.1, 13.5 +/- 4.4, 8.2 +/- 4.4, respectively, in those with ACS. The numbers of myocardial segments that did not uptake 99mTc-tetrofosmin during the acute phase were 0.5 +/- 0.8 and 3.6 +/- 2.8 in patients with Takotsubo cardiomyopathy and ACS, respectively. Impaired coronary microcirculation might be a causative mechanism of Takotsubo cardiomyopathy.

                Author and article information

                S. Karger AG
                August 2007
                24 October 2006
                : 108
                : 2
                : 144-146
                St. Vincent Hospital, Worcester, Mass., USA
                96476 Cardiology 2007;108:144–146
                © 2007 S. Karger AG, Basel

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                References: 15, Pages: 3
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