Left ventricular free wall rupture (LVFWR) is a rare and fatal mechanical complication following an acute myocardial infarction (AMI). Cases of survival after LVFWR due to ST-segment elevation myocardial infarction (STEMI) treated with a conservative treatment strategy are extremely rare. In this case, a 55-year-old male patient with several cardiovascular risk factors presented to the emergency department with symptoms of ongoing chest pain and syncope. The patient's electrocardiogram was in sinus rhythm with ST-elevation on I, aVL, and V4-6 leads. His myoglobin and troponin I levels were elevated. Due to the unstable hemodynamic state of the patient, bedside echocardiography was performed. The echocardiography indicated LVFWR after AMI. Pericardiocentesis was used to restore a satisfactory hemodynamic state in the patient. Following the initial treatment, the patient opted for a conservative treatment strategy and was uneventfully discharged after 19 days.
Background Heart rate acceleration and deceleration capacities are novel parameters that can quantify sympathetic and vagal modulation. However, how acceleration and deceleration capacities associated with circadian blood pressure (BP) variation remains unknown. Methods A total of 141 patients with essential hypertension were included in our study. Based on the nocturnal decline rate of systolic BP (SBP), patients were divided into two groups, as dippers and nondippers. Baseline demographic characteristics, ambulatory blood pressure monitoring (ABPM) parameters, Holter recordings, and echocardiographic parameters were collected. Results The absolute values of acceleration capacity (AC) (−7.75 [−8.45 ~ −6.3] ms vs. −6.6 [−8.25 ~ −5.2] ms, p = .047) and deceleration capacity (DC) (7.35 [6.1 ~ 8.1] ms vs. 6.3 [5.1 ~ 7.6] ms, p = .042) were significantly higher in dippers than in nondippers. By multivariate logistic regression analysis, left atrial diameter (LAd) was found to be an independent risk factor for nondipper status in acceleration capacity model (odds ratio 1.174, 95% confidence interval 1.019–1.354, p = .027) and deceleration model (odds ratio 1.146, 95% confidence interval 1.003–1.309, p = .045). Sleep SBP was positively correlated to acceleration capacity ( r = .256, p = .002) and negatively correlated to deceleration capacity ( r = −.194, p = .021). Conclusions The absolute values of acceleration capacity and deceleration capacity were higher in patients with dipper hypertension than in patients with nondipper hypertension. However, acceleration and deceleration capacities were not independent risk factors for blunted BP variation. Sleep SBP seemed to be better correlated to the impairment of autonomic nervous system (ANS) function than other ABPM parameters.
Background: Emerging evidence indicates the role of gut microbiota in the development of cardiovascular diseases. Thus, gut microbiota is increasingly recognized as a potential therapeutic target of cardiovascular disease. However, the effects of gut microbiome-targeted therapies on cardiometabolic outcomes in children and adolescents remain unclear. Methods: We plan to perform a systematic search from PubMed, EMBASE, Cochrane Central Register of Controlled Trials, and Web of Science. Two authors will independently select the relevant studies and extract data according to a previously defined data extraction sheet. We will use the Stata 14.0 statistical software and RevMan V.5.3 software to conduct data analyses. Results and conclusion: The results of this study will be published in a peer-reviewed journal and provide more evidence for the application of gut microbiome-targeted therapies in children and adolescents for the intervention of cardiovascular risk factors in clinical practice. Protocol registration number: INPLASY202060050.
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