BACKGROUND: Takotsubo cardiomyopathy (TTC) is increasingly well-recognized as a cause of chest-pain syndromes, especially in aging females. The most common complications of TTC occur in the first 24 hours post onset of symptoms and include shock and/or arrhythmias. HYPOTHESIS: We tested the hypothesis that the severity of early hypotension in TTC reflects the extent of myocardial involvement and dysfunction. METHODS: In 80 consecutive TTC patients, correlates of blood pressure on the day of admission were sought via univariate followed by multivariate analysis. RESULTS: Mean systolic blood pressure (SBP) on day 1 was 120 ± 24 (SD) mm Hg. During the first 3 days of admission, 39% of patients had SBP <90 mm Hg, and 9% died and/or required intra-aortic balloon pump insertion. The extent of release of N-terminal pro-brain natriuretic peptide, with its potential correlate of associated vasodilator activity, varied inversely with pulmonary-artery saturation, a measure of cardiac output. However, there was no significant relationship between normetanephrine release and SBP. On multivariate analyses there was no significant relationship between SBP and (1) wall-motion score index (as an index of left-ventricular systolic dysfunction) or (2) T2 enhancement on cardiac magnetic resonance imaging and peak N-terminal pro-brain natriuretic peptide (as indices of myocardial inflammation). CONCLUSIONS: Although severe hypotension and shock occur commonly during acute stages of TTC, these complications are multifactorial in origin, probably representing a combination of impaired inotropic state and vasodilatation. Importantly, initial hypotension does not imply severe left ventricular inflammation or systolic dysfunction.
BACKGROUND:Takotsubo cardiomyopathy (TTC) is increasingly well-recognized as a cause of chest-pain syndromes, especially in aging females. The most common complications of TTC occur in the first 24 hours post onset of symptoms and include shock and/or arrhythmias. HYPOTHESIS: We tested the hypothesis that the severity of early hypotension in TTC reflects the extent of myocardial involvement and dysfunction. METHODS: In 80 consecutive TTC patients, correlates of blood pressure on the day of admission were sought via univariate followed by multivariate analysis. RESULTS: Mean systolic blood pressure (SBP) on day 1 was 120 ± 24 (SD) mm Hg. During the first 3 days of admission, 39% of patients had SBP <90 mm Hg, and 9% died and/or required intra-aortic balloon pump insertion. The extent of release of N-terminal pro-brain natriuretic peptide, with its potential correlate of associated vasodilator activity, varied inversely with pulmonary-artery saturation, a measure of cardiac output. However, there was no significant relationship between normetanephrine release and SBP. On multivariate analyses there was no significant relationship between SBP and (1) wall-motion score index (as an index of left-ventricular systolic dysfunction) or (2) T2 enhancement on cardiac magnetic resonance imaging and peak N-terminal pro-brain natriuretic peptide (as indices of myocardial inflammation). CONCLUSIONS: Although severe hypotension and shock occur commonly during acute stages of TTC, these complications are multifactorial in origin, probably representing a combination of impaired inotropic state and vasodilatation. Importantly, initial hypotension does not imply severe left ventricular inflammation or systolic dysfunction.
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