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Unrevealing Takotsubo syndrome. appraising what has emerged from the International journal of cardiology contributions in 2019
No full textTakotsubo Syndrome (TTS) has received much attention in recentyears because of its intriguing clinical presentation and pathophysiology [1]. It has been 27 years since Sato et al. described a clinical condition in which patients present with an abrupt angina-like chest pain and diffuse ST-segment changes in the absence of obstructive coronary artery disease (CAD) [1]. Although recent work has added several pieces to the complex puzzle of the pathophysiology of TTS (Fig. 1), multiple aspects remain unclear [2]. A number of articles published recently in the International Journal of Cardiology in 2019 have provided novel important contributions to our understanding of this condition
Imaging of cardiac adrenergic innervation
No full textDevelopment of radioactive tracers to probe both pre- and postsynaptic sympathetic function has made possible a more widespread non-invasive assessment of the sympathetic nervous system
Coronary vasodilator reserve in primary and secondary left ventricular hypertrophy - A study with positron emission tomography
No full textObjectives Coronary vasodilator reserve is reduced in hypertrophic cardiomyopathy and secondary left ventricular hypertrophy despite angiographically normal coronaries. The aim of the present study was to assess whether quantitative differences exist between these conditions. Methods Using positron emission tomography with (H2O)-O-15, myocardial blood flow was measured at baseline and following intravenous dipyridamole (0 . 56 mg.kg(-1)) in 12 hypertrophic cardiomyopathy patients (age 34 (11) years, mean (SD), all male), 16 secondary left ventricular hypertrophy patients (age 58 (20) years: P<0 . 01 vs hypertrophic cardiomyopathy; 10 female) and 40 normal controls (age 54 (20), 13 female). In view of the known decline of post-dipyridamole myocardial blood flow with age, myocardial blood flow was compared between the patient groups and appropriately matched subsets of the total control group. Results Baseline myocardial blood Bow in the hypertrophic cardiomyopathy patients was 0 . 82 (0 . 23) ml.min(-1).g(-1) vs 0 . 94 (0 . 14) ml.min(-1).g(-1) in its matched control group, P=ns. For the secondary left ventricular hypertrophy patient group, baseline myocardial blood flow was 1 . 17 (0 . 40) ml.min(-1).g(-1) vs 1 . 06 (0 . 28) ml.min(-1).g(-1) for the secondary left ventricular hypertrophy matched control group, P=ns. Following dipyridamole, myocardial blood flow was 1 . 64 (0 . 44) ml.min(-1).g(-1) in hypertrophic cardiomyopathy patients vs 3 . 50 (0 . 95) ml.min(-1).g(-1) for the hypertrophic cardiomyopathy matched control group, P=0 . 0001. For the left ventricular hypertrophy patients, post-dipyridamole myo-cardial blood flow was 2 . 27 (0 . 60) ml.min(-1).g(-1) vs 2 . 94 (1 . 29) ml.min(-1).g(-1) for the left ventricular hypertrophy controls, P=0 . 06. Coronary vasodilator reserve (dipyridamole-myocardial blood flow/baseline-myocardial blood flow) was 2 . 05 (0 . 61) for hypertrophic cardiomyopathy patients vs 3 . 81 (0 . 98) for the hypertrophic cardiomyopathy controls (P=0 . 0001, patients vs controls) and 2 . 06 (0 . 62) for left ventricular hypertrophy patients vs 2 . 90 (1 . 38) for the left ventricular hypertrophy controls, P<0 . 03 patients vs controls. After correction of baseline myocardial blood flow for baseline heart rate x systolic pressure product, coronary vasodilator reserve for the hypertrophic cardiomyopathy patients was 2 . 06 (1 . 06) vs 4 . 34 (1 . 54) for the hypertrophic cardiomyopathy controls, P=0 . 0002 and in the secondary left ventricular hypertrophy patients, the values were 2 . 13 (0 . 64) vs 2 . 89 (1 . 42) in the secondary left ventricular hypertrophy controls, P<0 . 05. Conclusion In both hypertrophic cardiomyopathy and secondary left ventricular hypertrophy, the computed coronary vasodilator reserve is impaired, even after correction for baseline cardiac work. However, the extent of the reduction is greater in the hypertrophic cardiomyopathy patients. In the blunting of vasodilator reserve of secondary left ventricular hypertrophy, the patients' greater hyperaemic response is partly offset by the higher baseline myocardial blood flow
MYOCARDIAL-METABOLISM IN ISCHEMIC HEART-DISEASE - BASIC PRINCIPLES AND APPLICATION TO IMAGING BY POSITRON EMISSION TOMOGRAPHY
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