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Management of Tako-tsubo syndrome.

Cardiovasc Drugs Ther. 2008 Feb;22(1):71-7

Authors: Tarkin JM, Khetyar M, Kaski JC

INTRODUCTION: This manuscript reviews the current evidence for proposed pathophysiological mechanisms of Tako-tsubo syndrome and its management. DISCUSSION: The Tako-tsubo syndrome is defined by the presence of transient left ventricular apical ballooning after an acute coronary syndrome in patients with angiographically normal coronary arteries. Intriguingly, only the apex is affected and compensatory basal hypercontractility is seen. Several mechanisms have been offered as explanations for the characteristic clinical presentation and echocardiographic appearance of this syndrome. CONCLUSION: Tako-tsubo syndrome encompasses heterogeneous patient populations and it is likely that different pathogenic mechanisms may operate in different patients. Treatment of the condition is at present empirical and aimed at preserving ventricular function.

PMID: 18165891 [PubMed - indexed for MEDLINE]

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Effect of beta-blockade and ACE inhibition on B-type natriuretic peptides in stable patients with systolic heart failure.

Cardiovasc Drugs Ther. 2008 Aug;22(4):305-11

Authors: Rosenberg J, Gustafsson F, Remme WJ, Riegger GA, Hildebrandt PR

INTRODUCTION: The long-term effect of beta-blockade on the plasma levels of natriuretic peptides BNP and its N-terminal counterpart, NT-proBNP, as risk markers in heart failure (HF) is obscure. METHODS: Stable systolic HF patients from the CARMEN study were divided in groups matching their randomised treatment allocation: Carvedilol, enalapril or carvedilol+enalapril. Changes in BNP and NT-proBNP from baseline to 6 months maintenance visit were evaluated in each treatment arm. Furthermore, the prognostic value of BNP and NT-proBNP during monotherapy with carvedilol was assessed with univariate Cox proportional hazards models using a combined endpoint of all cause mortality and cardiovascular hospitalisation. RESULTS: NT-proBNP and BNP were significantly reduced after six months treatment with enalapril (NT-proBNP 1,303 to 857 pg/ml (P < 0.001), BNP 119 to 85 pg/ml (P < 0.001)) or carvedilol+enalapril (NT-proBNP 1,223 to 953 pg/ml (P = 0.003), BNP 117 to 93 pg/ml (P = 0.01)). In contrast, no change was observed in the carvedilol group (NT-proBNP 907 to 1,082 pg/ml (P = 0.06), BNP 114 to 130 pg/ml (P = 0.15). The prognostic value of NT-proBNP and BNP was maintained in the carvedilol group (NT-proBNP HR 1.018 95% CI (1.005-1.032), BNP 1.171 (1.088-1.260)). CONCLUSION: Treatment of HF patients with carvedilol alone does not reduce levels of natriuretic peptides, but treatment with enalapril does. Both BNP and NT-proBNP predict death and hospitalisation in HF patients treated with carvedilol for six months. The clinical implication of our results is that NT-proBNP and BNP can be used as risk markers of death and cardiovascular hospitalisations in systolic HF patients receiving carvedilol without ACE inhibition.

PMID: 18309461 [PubMed - indexed for MEDLINE]

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