Transient Ventricular Dysfunction Syndrome

Response To the Editor: I thank Lippi and Targher for their kind remarks about my editorial in CHEST (February 2008),1 which describes “tricks of the trade” for assessing pulmonary embolism prognosis. They raise two important questions: (1) Should measurement of natriuretic peptides such as brain natriuretic peptide or pro-brain natriuretic peptide be incorporated into routine prognostic assessment of acute pulmonary embolism? (2) Do brain natriuretic peptide levels provide clinically useful, complementary information ahove and beyond troponin measurement? Troponin measurement has several advantages over natriuretic peptides. First, any elevation of troponin, even a “troponin leak,” carries a markedly increased adverse prognosis for survival over the ensuing 30 days. Second, troponin as a pulmonary embolism biomarker has been far more extensively studied than natriuretic peptides. Third, the normal range for natriuretic peptides and the level at which they indicate a poor prognosis for pulmonary embolism remain uncvrtain. Fourth, the negative predictive value for a normal troponin level is almost 100%.Therefore, it is hard to conceive how natriuretic peptides can yield incrementally useful clinical information to indicate a favorable prognosis. Fifth, dissecting the contribution of occult or overt concomitant heart failure to elevated natriuretic peptide levels in the presence of pulmonary embolism is difficult. For now, we know that normal troponin levels indicate a likely excellent prognosis. I hope that some day soon, we will be able to use the combination of elevated troponin levels plus elevated natriuretic peptide levels as an indicator of an especially ominous prognosis. However, that day has not yet amved. Therefore, routine measurement of natriuretic peptides is not quite ready for prime time when assessing the prognosis of a patient with acute pulmonary embolism. Samuel Z . Goldhaber, MD, FCCP Boston, MA

The author has no conflict of interest to disclose. Reproduction of this article is rohibited without written permission from the American College ofchest Physicians (wwwchestjournal. orgmisdre rints.shtm1). Correspn&nce to: Samuel Z . Goldhaber, MD, FCCP, Cardiovascular Division, Brighani and Women’sHo ital, 75 Francis St, Boston, MA 02115-6110;e-mail: sgo1dhabe~partners.org DOI: 10.1378/chest.08-0495

drome.”’ The description of this novel syndrome has suffered with the lack of a consistent nomenclature and its everevolving picture through various reports, including the present one. For example, many case reports and case series on right ventricular involvement with a similar regional distribution as the left side have been published.”s Elesber et a14 were the first to describe it on a large scale. In their study published on 2S patients with transient left ventricular apical ballooning syndrome, 8 were found to have significant transient right ventricular apical involvement on echocardiography and it was associated with a longer and critical hospitalization. Haghi et a16 reported 9 of 34 patients (26%)with tako-tsubo cardiomyopathy with regional motion abnormalities in right ventricle (visualized on cardiac MRI). In eight of nine such patients, these segmental abnormalities cleared up with follow-up. Of note, the patients also had high incidence of certain underlying conditions (systemic hypertension, hypercholesteroleinia, diabetes, Graves’ disease, COPD and paroxysmal atrial fibrillation) which have the potential to adversely affect global right ventricular function. Yet, the finding seems significantly important with abnormalities being more regional and transient in nature. The distinction may be important for at least two reasons. First, the disorder affects more “globally” than it was earlier thought and second, right-sided involvement signifies a more severe impairment in left ventricular systolic function and poorer short-term prognosis as suggested by these reports. To conclude, it appears that “Transient Ventricular Dysfunction Syndrome” may thus be a more accurate choice instead of “Transient Left Ventricular Dysfunction Syndrome” in the face of existing evidence.

Nishith K. Sfngh, MD Southern I h J i s University School of Medidne Springfield, IL The author has no conflict of interest to disclose. Reproduetion of this article is rohibited without written permission h m the American College ofchest Physicians (www.chestjoumal. org/misdre rintsshtml). Correspon&nce to: Nkhith K Stngh, MD, 1617 Westchester Blvd 2, Springfield IL 62704; e-mail: nishith-singh2007@yahoo. con, [email protected] DOI: 10.1378/chest,07-3113

REFERENCES REFERENCE 1 Goldhaber SZ. Assessing the prognosis of acute pulmonary embolism: tricks of the trade. Chest 2008; 133:334-336

Transient Ventricular Dysfunction Syndrome The Evolving Nomenclature To the Editor: I would like to congratulate Kurowski and colleagues on their excellent work on tako-tsubo cardiomyopathy and the proposal of “Transient Left Ventricular Dysfunction Syn1532

Kurowski V, Kaiser A, von Hof K, et al. Apical and midventricular transient left ventricular dysfunction syndrome (takotsubo cardiomyopathy): frequency, mechanisms, and prognosis. Chest 2007: 132:809-816 Novak G , Kross K, Follmer K, et al. Transient biventricular apical ballooning: a unique presentation of the ‘broken heart.’ Chn Cardiol2007; 30:355-358 Nishikawa S, Ito K, Adachi Y, et al. Ampulla (‘takotsubo’) cardiomyopath of both ventricles: evaluation of niicrocirculation distur ance using 99mTc-tetrofosmin myocardial single photon emission computed tomography and Doppler guide wire. Circ J 2004; 68:1076-1080 Elesber AA, Prasad A, Byhee KA, et al. Transient cardiac apical ballooning syndrome: prevalence and clinical implications of right ventricular involvement. J Am Coll Cardiol 2006; 47:1082-1083 Haghi D, Athanasiadis A, Papavassiliu T, et al. Right ventricular involvement in takotsubo cardiomyopathy. Eur Heart J 2006: 27:2433-2439

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