Myocardial Stunning Due to Sudden Emotional Stress
http://www.100md.com
《新英格兰医药杂志》
To the Editor: Wittstein et al. (Feb. 10 issue)1 report a marked elevation of circulating markers of sympathetic stimulation, including neuropeptide Y, and raise the possibility of direct, catecholamine-induced myocardial stunning. Notable features of this syndrome are a presentation with chest pain and reversible electrocardiographic (ECG) abnormalities, which strongly suggest that severe, persistent myocardial ischemia is a cause of prolonged stunning.
Persistent, deep, negative T waves and reversible Q waves are common in patients with variant angina after very prolonged coronary spasm.2 In persons with stress-induced myocardial stunning, epicardial coronary-artery spasm has been documented angiographically by chance3 and after provocative tests.4 Moreover, my colleagues and I have shown that in humans, intracoronary injection of neuropeptide Y causes profound distal-vessel constriction, manifested as extremely slow flow, and massive ischemia.5 Thus, like all clinical syndromes, stress-induced myocardial stunning may have multiple causes. The role of spasm and distal-vessel constriction can be assessed only by performing arteriography during, rather than after, chest pain and by assessing the beneficial effects of intracoronary nitroprusside.
Attilio Maseri, M.D.
University Vita-Salute San Raffaele
20132 Milan, Italy
maseri.attilio@hsr.it
References
Wittstein IS, Thiemann DR, Lima JAC, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539-548.
Maseri A, Severi S, Nes MD, et al. "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia: pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol 1978;42:1019-1035.
Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472-479.
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
Clarke JG, Davies GJ, Kerwin R, et al. Coronary artery infusion of neuropeptide Y in patients with angina pectoris. Lancet 1987;1:1057-1059.
To the Editor: Wittstein et al. describe the clinical and ECG features of left ventricular dysfunction related to emotional stress. These stress-related phenomena have been recognized in Japan and have been called the tako-tsubo syndrome.1,2 Wittstein et al. report that only 2 of their 19 patients (11 percent) had ST-segment elevation on the initial ECG. In contrast, we recently described the ECG time course of the tako-tsubo syndrome as follows.2 ST-segment elevation is typical, especially in leads V3 through V6 shortly after the onset of symptoms. T-wave inversion deepens progressively to its first negative peak, which occurs at approximately three days. The T wave is shallow for several days and then deepens again; the second negative peak occurs at approximately two to three weeks. The QT interval is prolonged as the T wave deepens and shortens as the T wave becomes shallow. Repeated deepening of the T wave does not mean the recurrence or worsening of this syndrome.
Satoshi Kurisu, M.D.
Ichiro Inoue, M.D.
Takuji Kawagoe, M.D.
Hiroshima City Hospital
Hiroshima 730-8518, Japan
skurisu@nifty.com
References
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
Kurisu S, Inoue I, Kawagoe T, et al. Time course of electrocardiographic changes in patients with tako-tsubo-like syndrome: comparison with acute myocardial infarction with minimal enzymatic release. Circ J 2004;68:77-81.
To the Editor: Wittstein and colleagues demonstrate the probable role played by massive release of catecholamines in the pathogenesis of stress-induced cardiomyopathy. I would like to draw attention to a very similar clinicopathological syndrome resulting from scorpion envenomation, especially after stings by the Indian red scorpion (Mesobuthus tamulus) and the Brazilian scorpion (Tityus serrulatus).1,2 This syndrome is characterized by a late adrenergic phase associated with transient impairment of myocardial contractility due to toxic myocarditis, resulting in pulmonary edema and electrocardiographic changes akin to those of stress-induced cardiomyopathy. Contraction-band myocyte necrosis similar to that observed by Wittstein et al. has also been well documented in cases of scorpion envenomation.2,3 This analogy provides further support for the etiologic role played by catecholamines in the pathogenesis of stress-induced cardiomyopathy. Moreover, the alpha-adrenergic blocker prazosin reduces the risk of pulmonary edema and the risk of death in persons with scorpion envenomation.4 Apart from causing vasodilatation, alpha-adrenergic blockade by prazosin probably provides myocardial protection and might be beneficial in stress-induced cardiomyopathy as well.
Tamilarasu Kadhiravan, M.D.
All India Institute of Medical Sciences
New Delhi 110029, India
kadhiravant@yahoo.co.in
References
Bawaskar HS, Bawaskar PH. Cardiovascular manifestations of severe scorpion sting in India (review of 34 children). Ann Trop Paediatr 1991;11:381-387.
Cupo P, Jurca M, Azeedo-Marques MM, Oliveira JS, Hering SE. Severe scorpion envenomation in Brazil: clinical, laboratory and anatomopathological aspects. Rev Inst Med Trop Sao Paulo 1994;36:67-76.
Benvenuti LA, Douetts KV, Cardoso JL. Myocardial necrosis after envenomation by the scorpion Tityus serrulatus. Trans R Soc Trop Med Hyg 2002;96:275-276.
Bawaskar HS, Bawaskar PH. Severe envenoming by the Indian red scorpion Mesobuthus tamulus: the use of prazosin therapy. QJM 1996;89:701-704.
The authors reply: Although a marked elevation in plasma catecholamine levels appears to underlie the mechanism of stress-induced myocardial stunning, it is not known whether stunning results from catecholamine-mediated vasoconstriction or from the direct effects of catecholamines on cardiac myocytes. Dr. Maseri highlights some of the arguments for the potential role of coronary vasoconstriction in the pathogenesis of stress cardiomyopathy, including substantial elevations in potent vasoconstrictors, such as neuropeptide Y, and the observation by others that patients with this syndrome frequently have coronary spasm in response to provocative maneuvers. We have not used provocative maneuvers at our center, but we have performed coronary angiography in dozens of patients with stress cardiomyopathy, including several with chest pain and ST-segment elevation at the time of the angiographic study, and have never observed epicardial spasm. However, we have frequently observed decreased epicardial flow in the absence of fixed stenoses — a finding that suggests a possible role of microcirculatory dysfunction in the pathogenesis of this syndrome.1 We have also seen cases of true multivessel epicardial vasospasm that differed from stress cardiomyopathy in that the spasm was readily apparent and was associated with a substantial release of cardiac enzymes. Furthermore, neither the classic pattern of left ventricular apical ballooning nor the marked elevation in catecholamines observed with stress cardiomyopathy developed in these patients.
In response to Dr. Kurisu and colleagues: we agree that physicians should be familiar with the ECG changes associated with this syndrome, which include QT-interval prolongation and deep T-wave inversion that evolve during the first two to three hospital days. Frequently, the ECG continues to show abnormalities long after left ventricular function has normalized, and we agree that the repeated deepening of the T wave at two to three weeks is not associated with clinical or left ventricular deterioration. Physicians should also be aware that the ECG obtained at the time of admission can be quite variable. In the largest Japanese series of patients with left ventricular apical ballooning, 90 percent of the patients had ST-segment elevation.2 This finding is in contrast to the less frequent observation of ST-segment elevation in our experience and that reported by others.3,4
We thank Dr. Kadhiravan for highlighting the clinical features of scorpion envenomation. Many of the cardiac abnormalities seen with this catecholamine-mediated disorder are similar to those observed with stress cardiomyopathy. The observation that prazosin may reduce the risk of pulmonary edema and death after a scorpion sting suggests that adrenergic blockade may indeed have a role in the management of stress cardiomyopathy.
Ilan S. Wittstein, M.D.
Hunter C. Champion, M.D., Ph.D.
Johns Hopkins University School of Medicine
Baltimore, MD 21287
iwittste@jhmi.edu
References
Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343-346.
Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-18.
Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart 2003;89:1027-1031.
Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472-479.
Persistent, deep, negative T waves and reversible Q waves are common in patients with variant angina after very prolonged coronary spasm.2 In persons with stress-induced myocardial stunning, epicardial coronary-artery spasm has been documented angiographically by chance3 and after provocative tests.4 Moreover, my colleagues and I have shown that in humans, intracoronary injection of neuropeptide Y causes profound distal-vessel constriction, manifested as extremely slow flow, and massive ischemia.5 Thus, like all clinical syndromes, stress-induced myocardial stunning may have multiple causes. The role of spasm and distal-vessel constriction can be assessed only by performing arteriography during, rather than after, chest pain and by assessing the beneficial effects of intracoronary nitroprusside.
Attilio Maseri, M.D.
University Vita-Salute San Raffaele
20132 Milan, Italy
maseri.attilio@hsr.it
References
Wittstein IS, Thiemann DR, Lima JAC, et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med 2005;352:539-548.
Maseri A, Severi S, Nes MD, et al. "Variant" angina: one aspect of a continuous spectrum of vasospastic myocardial ischemia: pathogenetic mechanisms, estimated incidence and clinical and coronary arteriographic findings in 138 patients. Am J Cardiol 1978;42:1019-1035.
Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472-479.
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
Clarke JG, Davies GJ, Kerwin R, et al. Coronary artery infusion of neuropeptide Y in patients with angina pectoris. Lancet 1987;1:1057-1059.
To the Editor: Wittstein et al. describe the clinical and ECG features of left ventricular dysfunction related to emotional stress. These stress-related phenomena have been recognized in Japan and have been called the tako-tsubo syndrome.1,2 Wittstein et al. report that only 2 of their 19 patients (11 percent) had ST-segment elevation on the initial ECG. In contrast, we recently described the ECG time course of the tako-tsubo syndrome as follows.2 ST-segment elevation is typical, especially in leads V3 through V6 shortly after the onset of symptoms. T-wave inversion deepens progressively to its first negative peak, which occurs at approximately three days. The T wave is shallow for several days and then deepens again; the second negative peak occurs at approximately two to three weeks. The QT interval is prolonged as the T wave deepens and shortens as the T wave becomes shallow. Repeated deepening of the T wave does not mean the recurrence or worsening of this syndrome.
Satoshi Kurisu, M.D.
Ichiro Inoue, M.D.
Takuji Kawagoe, M.D.
Hiroshima City Hospital
Hiroshima 730-8518, Japan
skurisu@nifty.com
References
Kurisu S, Sato H, Kawagoe T, et al. Tako-tsubo-like left ventricular dysfunction with ST-segment elevation: a novel cardiac syndrome mimicking acute myocardial infarction. Am Heart J 2002;143:448-455.
Kurisu S, Inoue I, Kawagoe T, et al. Time course of electrocardiographic changes in patients with tako-tsubo-like syndrome: comparison with acute myocardial infarction with minimal enzymatic release. Circ J 2004;68:77-81.
To the Editor: Wittstein and colleagues demonstrate the probable role played by massive release of catecholamines in the pathogenesis of stress-induced cardiomyopathy. I would like to draw attention to a very similar clinicopathological syndrome resulting from scorpion envenomation, especially after stings by the Indian red scorpion (Mesobuthus tamulus) and the Brazilian scorpion (Tityus serrulatus).1,2 This syndrome is characterized by a late adrenergic phase associated with transient impairment of myocardial contractility due to toxic myocarditis, resulting in pulmonary edema and electrocardiographic changes akin to those of stress-induced cardiomyopathy. Contraction-band myocyte necrosis similar to that observed by Wittstein et al. has also been well documented in cases of scorpion envenomation.2,3 This analogy provides further support for the etiologic role played by catecholamines in the pathogenesis of stress-induced cardiomyopathy. Moreover, the alpha-adrenergic blocker prazosin reduces the risk of pulmonary edema and the risk of death in persons with scorpion envenomation.4 Apart from causing vasodilatation, alpha-adrenergic blockade by prazosin probably provides myocardial protection and might be beneficial in stress-induced cardiomyopathy as well.
Tamilarasu Kadhiravan, M.D.
All India Institute of Medical Sciences
New Delhi 110029, India
kadhiravant@yahoo.co.in
References
Bawaskar HS, Bawaskar PH. Cardiovascular manifestations of severe scorpion sting in India (review of 34 children). Ann Trop Paediatr 1991;11:381-387.
Cupo P, Jurca M, Azeedo-Marques MM, Oliveira JS, Hering SE. Severe scorpion envenomation in Brazil: clinical, laboratory and anatomopathological aspects. Rev Inst Med Trop Sao Paulo 1994;36:67-76.
Benvenuti LA, Douetts KV, Cardoso JL. Myocardial necrosis after envenomation by the scorpion Tityus serrulatus. Trans R Soc Trop Med Hyg 2002;96:275-276.
Bawaskar HS, Bawaskar PH. Severe envenoming by the Indian red scorpion Mesobuthus tamulus: the use of prazosin therapy. QJM 1996;89:701-704.
The authors reply: Although a marked elevation in plasma catecholamine levels appears to underlie the mechanism of stress-induced myocardial stunning, it is not known whether stunning results from catecholamine-mediated vasoconstriction or from the direct effects of catecholamines on cardiac myocytes. Dr. Maseri highlights some of the arguments for the potential role of coronary vasoconstriction in the pathogenesis of stress cardiomyopathy, including substantial elevations in potent vasoconstrictors, such as neuropeptide Y, and the observation by others that patients with this syndrome frequently have coronary spasm in response to provocative maneuvers. We have not used provocative maneuvers at our center, but we have performed coronary angiography in dozens of patients with stress cardiomyopathy, including several with chest pain and ST-segment elevation at the time of the angiographic study, and have never observed epicardial spasm. However, we have frequently observed decreased epicardial flow in the absence of fixed stenoses — a finding that suggests a possible role of microcirculatory dysfunction in the pathogenesis of this syndrome.1 We have also seen cases of true multivessel epicardial vasospasm that differed from stress cardiomyopathy in that the spasm was readily apparent and was associated with a substantial release of cardiac enzymes. Furthermore, neither the classic pattern of left ventricular apical ballooning nor the marked elevation in catecholamines observed with stress cardiomyopathy developed in these patients.
In response to Dr. Kurisu and colleagues: we agree that physicians should be familiar with the ECG changes associated with this syndrome, which include QT-interval prolongation and deep T-wave inversion that evolve during the first two to three hospital days. Frequently, the ECG continues to show abnormalities long after left ventricular function has normalized, and we agree that the repeated deepening of the T wave at two to three weeks is not associated with clinical or left ventricular deterioration. Physicians should also be aware that the ECG obtained at the time of admission can be quite variable. In the largest Japanese series of patients with left ventricular apical ballooning, 90 percent of the patients had ST-segment elevation.2 This finding is in contrast to the less frequent observation of ST-segment elevation in our experience and that reported by others.3,4
We thank Dr. Kadhiravan for highlighting the clinical features of scorpion envenomation. Many of the cardiac abnormalities seen with this catecholamine-mediated disorder are similar to those observed with stress cardiomyopathy. The observation that prazosin may reduce the risk of pulmonary edema and death after a scorpion sting suggests that adrenergic blockade may indeed have a role in the management of stress cardiomyopathy.
Ilan S. Wittstein, M.D.
Hunter C. Champion, M.D., Ph.D.
Johns Hopkins University School of Medicine
Baltimore, MD 21287
iwittste@jhmi.edu
References
Bybee KA, Prasad A, Barsness GW, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004;94:343-346.
Tsuchihashi K, Ueshima K, Uchida T, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. J Am Coll Cardiol 2001;38:11-18.
Desmet WJ, Adriaenssens BF, Dens JA. Apical ballooning of the left ventricle: first series in white patients. Heart 2003;89:1027-1031.
Sharkey SW, Lesser JR, Zenovich AG, et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation 2005;111:472-479.