Letter by Madias Regarding Article, “Systolic and Diastolic Mechanics in Stress Cardiomyopathy”
To the Editor:
I enjoyed reading the study by Medeiros et al1 comparing left ventricular (LV) systolic and diastolic mechanics in 24 patients with the Takotsubo syndrome (TTS), 36 patients with an acute left anterior descending coronary artery territory myocardial infarction (LAD MI), and 30 control subjects with no coronary artery or other cardiac diseases. The authors limited their investigation to women in their early 60s, and they evaluated LV mechanics using hemodynamic and angiographic studies during cardiac catheterization and transthoracic echocardiography. Because the cause of LAD MI is regional myocardial ischemic injury and that of TTS is currently ascribed to primary activation of the autonomic sympathetic nervous system resulting in widespread myocardial injury, with permanent residual damage in the former and full recovery in the latter, the authors expected different LV mechanics in LAD MI and TTS. To their surprise, they documented similarly elevated LV diastolic pressures, diastolic stiffness, LV systolic volumes, and abnormal contractility indexes and ventricular-arterial coupling in LAD MI and TTS patients compared with the control subjects but no differences between LAD MI and TTS patients. Experience with TTS (http://www.ncbi.nlm.nih.gov/pubmed/?term=takotsubo) reveals that LV diastolic pressures in many patients are normal or even low, in variance with the present study. An explanation for this difference may be that the patients with TTS were studied relatively late after onset of their illness; information is provided about the cardiac catheterization being carried out an average of 97.3 minutes after the patients with LAD MI arrived at the hospital, whereas the patients with TTS were studied at “24 to 48 hours after presentation.” TTS is characterized by major changes in hemodynamics and other attributes during this long time period; thus, the findings of this study amount to a snapshot assessment of the LV mechanics of patients with TTS and are not reflective of the entire acute/subacute phase of the disease. A clue that this is the case is found in Table 2, where the average brain natriuretic peptide was reported as being 813.8 pg/dL in the patients with TTS and 865.4 pg/dL in the patients with LAD MI. According to experience (http://www.ncbi.nlm.nih.gov/pubmed/?term=takotsubo), values of brain natriuretic peptide are much higher in patients with TTS than in those with LAD MI, and they tend to drop rapidly in the former hours to 1 day after admission. Thus, the similar values of brain natriuretic peptide in these 2 cohorts imply that the patients with TTS underwent cardiac catheterization late in their clinical course.
I agree with the authors that “the similarity of these phenotypes [of patients with TTS and LAD MI] suggests the controversial hypothesis that some of the LV dysfunction with acute ischemic injury (LAD MI) may be due to catecholamine injury,” and I have gone even further to speculate that there may be a frequent TTS-like component in patients with an acute MI (transient LV wall motion abnormalities in the contralateral to the infarcted myocardial territory)2 and have included cases with acute coronary syndromes and TTS as comorbidities in newly proposed diagnostic criteria of TTS.3
John E. Madias, MD
Icahn School of Medicine at Mount Sinai
New York, NY
- © 2015 American Heart Association, Inc.