41,845 research outputs found
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
Coronary microvascular dysfunction: mechanisms and functional assessment.
No full textAbstract | Obstructive disease of the epicardial coronary arteries was recognized as the cause of angina pectoris >2 centuries ago, and sudden thrombotic occlusion of an epicardial coronary artery has been established as the cause of acute myocardial infarction for >100 years. In the past 2 decades, dysfunction of the coronary microvasculature emerged as an additional mechanism of myocardial ischaemia that bears important prognostic implications. The coronary microvasculature (vessels <300 μm in diameter) cannot be directly imaged in vivo, but a number of invasive and noninvasive techniques, each with relative advantages and pitfalls, can be used to assess parameters that depend directly on coronary microvascular function. These methods include invasive or noninvasive measurement of Doppler-derived coronary blood flow velocity reserve, assessment of myocardial blood flow and flow reserve using noninvasive imaging, and calculation of microcirculatory resistance indexes during coronary catheterization. These advanced techniques for assessment of the coronary microvasculature have provided novel insights into the pathophysiological role of coronary microvascular dysfunction in the development of myocardial ischaemia in different clinical conditions
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
Relationship between right and left ventricle mass in uncomplicated systemic arterial hypertension: a study with cardiac magnetic resonance
No full textBackground: Systemic arterial hypertension (AH) is a common clinical condition associated with an increased risk for cardiovascular disease and death. Little is known about the involvement of the right ventricle at an early stage of the disease.
Our aim was: a) to assess the right and left ventricle volumes in hypertensive patients compared to a normotensive group by Cardiac Magnetic Resonance (CMR) b) to evaluate the right and left ventricle mass in hypertensive patients compared to a normotensive group by CMR c) to investigate if a relation between left and right ventricular mass exists.
Methods: Using CMR (1.5 Tesla, GE Healthcare, Milwaukee, USA) we evaluated right (RVM) and left ventricles mass (LVM), right (RVEDV) and left (LVEDV) end diastolic volume, right (RVEF) and left (LVEF) ejection fraction in a group of mild to moderate hypertensive patients (n=19, male: 13, mean age: 58±10), without other clinical cardiovascular and systemic disease. As control (C) we included 19 healthy normotensive patients (male: 12, mean age: 46±14).
Results: LVM was significantly higher in hypertensive patients than in controls (93±16 g/m2 vs. 62±11 g/m2, p< 0.001), while there were no significantly differences in LVEDV (77±16 ml/m2 vs. 79±14 ml/m2, p=ns), RVEDV (73±16 ml/m2 vs. 74±13 ml/m2, p=ns), LVEF (64±6% vs. 66±8%, p=ns) and RVEF (68±8% vs. 64±7%, p=ns). A statistically significant association was found between LVM and RVM only in the AH group (r=0.75, p<0.001). Hypertensive patients with hypertrophic left ventricle showed an increase in RVM comparing to controls (28±4 vs. 22±4 g/m2, p= 0.006).
Conclusions: from these data we conclude that right ventricle is not an innocent bystander but it could be early involved in cardiac remodeling before a pressure overload is established in pulmonary circulation. The lack of significant relationship between LVM and RVM in control group, suggest a role of AH in the mechanism of right ventricle remodeling. However, more studies and investigation are necessary before the clinical importance of this phenomenon can be addressed
Malignancy in patients with myocardial infarction and non-obstructive coronary arteries. a systematic review and meta-regression
No full textBackground: The significance of malignancy in patients with myocardial infarction and non-obstructive coronary arteries (MINOCA) is poorly defined. This study aimed at determining the prevalence of malignancy and its association with long-term outcome in MINOCA. Methods: We searched the MEDLINE, EMBASE, and CENTRAL databases up to March 31, 2020 to identify studies reporting data on malignancy in full. We performed a random effects meta-analysis of proportions and assessed statistical heterogeneity using the I2 statistic and meta-regression analysis. Results: A total of 9 studies including 26,636 patients (11,910 men and 14,726 women) were selected for the meta-analysis. Of them, 655 patients (2.5%) had a diagnosis of malignancy at presentation. Comparison of presenting features and outcome between patients with MINOCA and patients with myocardial infarction and coronary artery disease (MI-CAD) showed that malignancy was significantly more common in the former as compared with the latter (p = 0.019). During a median follow-up of 39 months, 2,081 patients with MINOCA died (7.8%). Meta-regression analysis demonstrated that long-term mortality was associated with left ventricular ejection fraction (p = 0.0001; coefficient: -0.001; 95% CI: from -0.002 to 0.002), malignancy at presentation (p = 0.01; coefficient: 0.001; 95% CI: from -0.001 to 0.001), and use of beta-blockers during follow-up (p = 0.03; coefficient: 0.001; 95% CI: from -0.000 to 0.001). Conclusion: This study shows that the prevalence of malignancy in patients with MINOCA is not trivial and is significantly greater than in patients with MI-CAD. Malignancy is significantly associated with an unfavorable long-term prognosis in MINOCA
Heterogeneity of resting and hyperemic myocardial blood flow in healthy humans
No full textObjective: Absolute myocardial blood flow (MBF) is not well-defined in large normal populations, and appears to be heterogeneous in both humans and animals. These factors contribute to the difficulties in defining resting MBF to hibernating myocardium. We therefore assessed absolute baseline and hyperemic MBF in a large population of normal humans. Methods: MBF was quantified by positron emission tomography with oxygen-15-labeled water at baseline and during hyperemia induced by either adenosine or dipyridamole in 131 men and 38 women, aged 21-86 (mean 46+/-12) years. MBF was corrected for workload using the rate-pressure product (RPP). Results: Uncorrected baseline MBF ranged from 0.590 to 2.050 (mean 0.985+/-0.230) ml/min/g (coefficient of variation=27%), and corrected MBF from 0.736 to 2.428 (mean 1.330+/-0.316) ml/min/g (coefficient of variation=24%). MBF in the inferior region was significantly (P<0.0001) lower than either the anterior or lateral regions. Baseline MBF in females was significantly (P<0.001) higher than in males. Conclusions: These results confirm the heterogeneity of MBF in normals and highlight the difficulty in establishing the lower limit of normal MBF. (C) 2001 Elsevier Science B.V. All rights reserved
Cardiac nociception
No full textMechanisms underlying cardiac pain are of major importance in cardiovascular medicine. In this review we address a fundamental clinical and experimental aspect. In particular neural circuitry involved justify a stepwise involvement of central structures responsible of reflex adjustments initiated by peripheral ischemia that can be associated with pain if a cortex is involved. Ischemic episodes not involving ascending neural circuits limited to the thalamus are not associated to pain. The same sensory inputs, when stimulated, may initiate positive feedback sympathetic reflexes from the heart
Mismatch between insulin-mediated glucose uptake and blood flow in the heart of patients with Type II diabetes
No full textAims/hypothesis. We investigated the effect of physiological hyperinsulinaemia on global and regional myocardial blood flow and glucose uptake in five patients with Type II (non-insulin-dependent) diabetes mellitus and seven healthy control subjects. Methods. Myocardial blood flow was assessed by positron emission tomography with oxygen-15 labelled water (H(2)(15)O) either before or after 1 h of euglycaemic hyperinsulinaemia. Myocardial glucose uptake was assessed by positron emission tomography and fluorine-18 labelled fluorodeoxyglucose ((18)FDG). Results. During hyperinsulinaemia, myocardial blood flow increased from 0.91 +/- 0.03 to 1.00 +/- 0.03 ml.min(-1).g(-1) in control subjects (p<0.005) and from 0.81 +/- 0.02 to 0.95 +/- 0.04 ml.min(-1).g(-1) in diabetic patients (p<0.0005). Corresponding glucose uptakes were 0.56 +/- 0.01 and 0.36 +/- 0.02 mumol.min(-1).g(-1) (p<0.0001), respectively. During hyperinsulinaemia, the regional distribution of myocardial blood flow and glucose uptake showed higher values in the septum and anterolateral wall (short axis) and in the mid-ventricle (long axis) in control subjects, and insulin action was circumscribed to these regions. In diabetic patients, the regional distribution of glucose uptake was similar; however, insulin-induced increase of myocardial blood flow was mainly directed to the postero-inferior areas (short axis) and to the base (long axis) of the heart, thus cancelling the predominance of the anterior wall observed before insulin administration. Conclusion/interpretation. These results provide evidence that insulin-mediated regulation of global myocardial blood flow is preserved in Type II diabetic patients. In contrast, the regional re-distribution of myocardial blood flow induced by insulin is directed to different target areas when compared with healthy subjects, thereby resulting in a mismatch between blood flow and glucose metabolism
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