© 2007 European Society of Cardiology
Pressure tracings in obstructive Tako-Tsubo cardiomyopathy
Department of Cardiology Hiroshima City Hospital 7-33, Moto-machi, Naka-ku, Hiroshima 730-8518, Japan
* Corresponding author. Tel.: +81 82 221 2291; fax: +81 82 223 1447. E-mail address: skurisu{at}nifty.com
| Abstract |
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A 70-year-old female experienced severe anxiety due to an incident with a stranger when she was home alone at night. Immediately after the event, she had an oppressive chest sensation; 16h later she was admitted to hospital. Left ventriculography showed akinesia of the mid-to-distal portion and hyperkinesia of the basal portion of the left ventricular chamber. However, coronary angiography showed no significant coronary artery disease. We diagnosed her as having Tako-Tsubo cardiomyopathy. Subsequently, left ventricular and central aortic pressures were recorded simultaneously. Initial recording showed a peak systolic gradient of 60mm Hg. On the first sinus beat after a premature ventricular contraction, the peak systolic gradient increased to 130mm Hg, and the pulse pressure decreased. Shortly after intravenous administration of nitroglycerin (0.5mg), central aortic pressure decreased and the peak systolic gradient increased to 100mm Hg. On the first sinus beat after a premature ventricular contraction, the peak systolic gradient increased to 160mm Hg, and the pulse pressure decreased. Five minutes after intravenous nitroglycerin, the peak systolic gradient returned to 70mm Hg. Follow-up transthoracic echocardiography 13days later showed normal left ventricular wall motion with no pressure gradient through the left ventricular outflow tract.
Key Words: Heart failure Elderly Gender Tako-Tsubo Pressure tracing
Received March 23, 2006; Accepted August 16, 2006
| 1. Introduction |
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Since Sato et al. first reported Tako-Tsubo cardiomyopathy in 1990 [1], this disorder has become accepted worldwide as a distinct clinical entity [2-5]. Recent studies have demonstrated that most patients are elderly women who experience emotional or physical stress antecedent to the onset. The mechanisms of Tako-Tsubo cardiomyopathy during early phase are complex and include left ventricular outflow tract (LVOT) obstruction, mitral regurgitation and arrhythmias.
We report a patient with Tako-Tsubo cardiomyopathy in whom LVOT obstruction was assessed by simultaneous tracings of left ventricular and central aortic pressures.
| 2. Case report |
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A 70-year-old female with diabetes and hypertension experienced severe anxiety due to an incident with a stranger when she was home alone at night. Immediately after the event, she had an oppressive chest sensation. Next day, she had dyspnoea on effort; she was admitted to our hospital 16 h after the onset of chest symptoms.
On admission, she was conscious, her blood pressure was 130/70 mm Hg, and pulse rate was 80 beats/min. A harsh 3/6 systolic murmur was noted over the apex and parasternal border. Her haematological test results, including creatine phosphokinase (92 U/L) and norepinephrine (407 pg/ml), were normal. Her chest X-ray showed mild pulmonary oedema and cardiac enlargement with a cardiothoracic ratio of 56%. Her ECG showed T wave inversion in leads I, II, aVF, V3-6 and transthoracic echocardiography showed akinesia of the mid-to-distal portion of the left ventricular chamber (Fig. 1). Left ventricular diastolic diameter was 46 mm. Interventricular wall thickness and posterior wall thickness were 14 mm and 8 mm, respectively. The pressure gradient through the LVOT, measured using continuous wave Doppler, was 96 mm Hg.
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After written informed consent was obtained, emergency cardiac catheterization was performed through the right femoral artery. Left ventriculography showed akinesia of the mid-to-distal portion and hyperkinesia of the basal portion of the left ventricular chamber. However, coronary angiography showed no significant coronary artery disease. We diagnosed Tako-Tsubo cardiomyopathy. Subsequently, left ventricular and central aortic pressures were recorded simultaneously (Fig. 2). Initial recording showed a peak systolic gradient of 60 mm Hg. On the first sinus beat after a premature ventricular contraction, the peak systolic gradient increased to 130 mm Hg, and the pulse pressure decreased. Shortly after intravenous administration of nitroglycerin (0.5 mg), central aortic pressure decreased and the peak systolic gradient increased to 100 mm Hg. On the first sinus beat after a premature ventricular contraction, the peak systolic gradient increased to 160 mm Hg, and the pulse pressure decreased. Five minutes after intravenous nitroglycerin, final recording showed that the peak systolic gradient returned to 70 mm Hg.
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The LVOT obstruction disappeared spontaneously 5 days later on follow-up echocardiography. Serial measurements of creatine phosphokinase were normal during the follow-up. No major adverse cardiac events occurred during the hospital stay, and the patient was discharged 7 days later. Follow-up transthoracic echocardiography at 13 days showed normal left ventricular wall motion with no pressure gradient through the LVOT.
| 3. Discussion |
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In the current report, we have demonstrated that the peak systolic gradient increased and the pulse pressure decreased on the first sinus beat after a premature ventricular contraction in obstructive Tako-Tsubo cardiomyopathy, using simultaneous tracings of left ventricular and central aortic pressures. This phenomenon was first found in obstructive hypertrophic cardiomyopathy, and is called the Brockenbrough-Braunwald-Morrow phenomenon [6-8]. The resultant increase in contractility on the first sinus beat after a premature ventricular contraction is so marked that it outweighs the otherwise salutary effect of increased ventricular filling caused by the compensatory pause and produces an increase in the gradient.
Although Maron et al. recently reported that LVOT obstruction is a strong, independent predictor of death in patients with hypertrophic cardiomyopathy [7], it does not seem to be associated with death in patients with Tako-Tsubo cardiomyopathy because it is usually transient. However, with LVOT obstruction, apical wall stress and left ventricular filling pressure increase while systemic blood pressure decreases, and these haemodynamic changes may cause heart failure and cardiogenic shock during the early phase of Tako-Tsubo cardiomyopathy.
Although positive inotropic agents are often used to treat heart failure or cardiogenic shock, these agents augment the peak systolic gradient by increasing myocardial contractility in patients with LVOT obstruction. Although nitroglycerin is also often used to treat heart failure, this exaggerates the gradient by decreasing arterial pressure and ventricular volume as shown in the current report. Thus, LVOT obstruction should be assessed during the early phase of Tako-Tsubo cardiomyopathy.
Beta-blockers, verapamil and disopyramide may be promising drugs for the treatment of LVOT obstruction in patients with Tako-Tsubo cardiomyopathy as well as in patients with hypertrophic cardiomyopathy. However, these two disorders are essentially different. Hypertrophic cardiomyopathy is characterised by normal systolic function, whereas in Tako-Tsubo cardiomyopathy systolic function is depressed. Since these drugs may make acute heart failure worse through a negative inotropic effect and LVOT obstruction is usually transient, these drugs should be used carefully in acute heart failure. Further studies are required to clarify appropriate strategies to treat heart failure or cardiogenic shock in patients with Tako-Tsubo cardiomyopathy complicated by LVOT obstruction.
| References |
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- Sato H., Tateishi H., Uchida T., Dote K., Ishihara M. Tako-Tsubo-like left ventricular dysfunction due to multivessel coronary spasm. In: Clinical aspect of myocardial injury: from ischemia to heart failure (in Japanese)—Kodama K., Haze K., Hori M., eds. (1990) Tokyo: Kagakuhyoronsha Publishing Co. 56–64.
- 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) 143:445–448.
- Desmet W.J., Adriaenssens B.F., Dens J.A. Apical ballooning of the left ventricle: first series in white patients. Heart (2003) 89:1027–1031.
[Abstract/Free Full Text] - Wittstein I.S., Thiemann D.R., Lima J.A., et al. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med (2005) 352:539–548.
[Abstract/Free Full Text] - Sharkey S.W., Lesser J.R., Zenovich A.G., et al. Acute and reversible cardiomyopathy provoked by stress in women from the United States. Circulation (2005) 111:472–479.
[Abstract/Free Full Text] - Brockenbrough E.C., Braunwald E., Morrow A.G. A hemodynamic technic for the detection of hypertrophic subaortic stenosis. Circulation (1961) 23:189–194.
[Abstract/Free Full Text] - Maron M.S., Olivotto L., Betocchi S., et al. Effect of left ventricular outflow tract obstruction on clinical outcome in hypertrophic cardiomyopathy. N Engl J Med (2003) 348:295–303.
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