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      Recurrent Apical Ballooning despite Treatment with Verapamil


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          Objective: To report a case of recurrent tako-tsubo syndrome that developed despite treatment with calcium channel antagonists. Case Summary: A 76-year-old woman with past medical history of ischemic heart disease and mild chronic asthma presented in 2001 with clinical characteristics and laboratory markers consistent with myocardial ischemia. Coronary angiogram was done with successful balloon angioplasty to LAD stenosis. Ventriculogram and echocardiography demonstrated apical ballooning believed to represent aneurysm formation. Several months later, a follow-up echocardiogram (ECG) revealed normal LV size and function with no wall motion abnormalities. ECG was unremarkable. In 2004, the patient was admitted with dyspnea, chest pain and ST elevation in ECG with normal troponin. Coronary angiogram demonstrated patent coronary tree. Left ventriculogram revealed apical ballooning sparing the base of the heart. Medically controlling the asthma attack led to clinical, echocardiographic and remarkable electrocardiographic normalization within days. Rest thallium perfusion scan done within 48 h demonstrated isolated fully reversible defect in the apex after 24 h suggesting a microvessel etiology. Conclusion: Tako-tsubo cardiomyopathy is an increasingly recognized condition. We report here the first case of tako-tsubo recurrence despite treatment with verapamil, and suggest a microvessel pathophysiology supported by rest thallium scan.

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          Most cited references 9

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          Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction.

          Peculiar asynergy, which consists of hypokinesis or akinesis from the mid portion to the apical area and hyperkinesis of the basal area on contrast left ventriculogram, is rare. Because the end-systolic left ventriculogram looks like a "tako-tsubo," which was used for trapping octopuses in Japan, we proposed the term "tako-tsubo-like left ventricular dysfunction." Our aim was to evaluate its clinical features and causes. We studied 30 patients with tako-tsubo-like left ventricular dysfunction without significant coronary artery disease. We assessed its pathophysiologic mechanisms by coronary spasm provocation test, endomyocardial biopsy, measurement of virus titer, and measurement of circulating catecholamine levels. Patient age ranged from 55 to 83 years. Twenty-eight were women and 2 were men. Tako-tsubo-like left ventricular dysfunction was dramatically resolved on predischarge left ventriculogram at 11.3 +/- 4.3 days. Acute coronary angiography revealed spontaneous multivessel coronary spasm in 3 patients. Among 14 patients, ergonovine or acetylcholine induced epicardial single coronary spasm in 4 patients and multivessel coronary spasm in 6 patients. Spontaneous microvascular spasm occurred at predischarge in 1 patient. An endomyocardial biopsy specimen in 3 patients and measurement of virus titer in 7 patients did not show evidence of acute myocarditis. Circulating norepinephrine was normal or slightly elevated in 6 patients. We showed clinical features of a novel cardiac syndrome with tako-tsubo-like left ventricular dysfunction. Although the precise cause remains unclear, simultaneous multivessel coronary spasm at the epicardial artery or microvascular levels may contribute to the onset of tako-tsubo-like left ventricular dysfunction.
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            Paradoxical release of nitric oxide by an L-type calcium channel antagonist, the R+ enantiomer of amlodipine.

            Amlodipine is a mixture of two enantiomers, one having L-type channel blocking activity (S-) and the other about 1,000-fold weaker activity and of little known other activity (R+). To determine whether the R+ enantiomer releases nitric oxide, the ability of amlodipine, its enantiomers, and nitrendipine to release nitric oxide in isolated coronary microvessels and to regulate cardiac tissue oxygen consumption via nitric oxide release was studied in vitro. Amlodipine and the R+ enantiomer released nitric oxide in a concentration-dependent fashion, increasing nitrite release from coronary microvessels by 57 +/- 12 and 45 +/- 5 pmol/mg/20 min at 10(-6) M (p < 0.05 from control). Nitrite release was entirely blocked by N(omega)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and HOE-140, a B2-kinin receptor antagonist. The S- enantiomer had no effect on nitrite release at any concentration. Amlodipine and the R+ enantiomer also reduced oxygen consumption in canine cardiac tissue in vitro and this was in an L-NAME-blockable manner. The S- enantiomer of amlodipine had no effect. This study shows that the R+ enantiomer of amlodipine is responsible for the release of nitric oxide and not the S- enantiomer (the L-type calcium channel blocking portion of amlodipine). Interestingly, nitric oxide release is dependent on the production of kinins because it is blocked by HOE-140. This study defines a potentially important property by which calcium channel blockers may release nitric oxide and may contribute to their use in the treatment of cardiovascular disease.
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              A Syndrome of Transient Left Ventricular Apical Wall Motion Abnormality in the Absence of Coronary Disease: A Perspective from the United States

              Background: The syndrome of chest pain associated with characteristic anterior electrocardiographic changes, moderate increases in cardiac enzymes, and a reversible apical wall motion abnormality in the absence of coronary artery disease has been documented in Japan, but has received relatively little attention in other countries. Methods: The clinical and echocardiographic data of 12 patients (11 women, mean age 64 ±14 years) who presented with chest symptoms, electrocardiographic (ECG) changes indicative of an acute anteroapical myocardial infarction, abnormal cardiac enzyme levels and echocardiography showing an apical wall motion abnormality were collected. Coronary angiography was performed in 10 patients. A follow-up echocardiogram was obtained within 2 weeks of the initial diagnosis in most cases. Results: An identifiable, precipitating (‘trigger’) event could be identified in all 12 individuals. Respiratory distress was present in 7, the death of a relative in 3, in 4 a surgical or medical procedure had been performed, and in 1 a panic disorder was diagnosed. The echocardiograms showed a characteristic wall motion pattern of significant apical dysfunction. All of the patients who underwent coronary arteriography had noncritical coronary artery disease. Follow-up echocardiography showed normalization of the LV dysfunction in all instances. Conclusion: We identified a syndrome of chest pain, dyspnea, ECG and enzyme changes mimicking acute myocardial infarction, similar to the ‘Takotsubo’ syndrome described in Japan. It is likely that the widespread use of echocardiography, coupled with increased recognition of this syndrome, will result in this diagnosis being made more commonly.

                Author and article information

                S. Karger AG
                September 2007
                07 November 2006
                : 108
                : 3
                : 210-213
                Departments of aInternal Medicine B, bCardiology, and cNuclear Medicine Unit, Hadassah, Hebrew University Medical Center, Jerusalem, Israel
                96779 Cardiology 2007;108:210–213
                © 2007 S. Karger AG, Basel

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                Figures: 4, References: 16, Pages: 4
                Case Report


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