In postmenopausal women the mechanisms responsible for hypertension have not been completely elucidated, and there are no gender-specific guidelines for women despite studies showing that blood pressure is not as well controlled to goal in women as in men. In the present study we tested the hypotheses that the sympathetic nervous system and the renal sympathetic nerves contribute to hypertension in aging female rats, that sympathetic activation may be mediated by the melanocortin 3/4 receptor (MC3/4R), and that MC3/4R activation may be due to increases in leptin. α-1, β-1,2-Adrenergic blockade reduced blood pressure in both young (3-4 mo) and old (18-19 mo) female spontaneously hypertensive rats (SHR). Renal denervation attenuated the hypertension more in old females than young females. MC3/4R antagonism with SHU-9119 given intracerebroventricularly had no effect on blood pressure in either young or old females but significantly reduced blood pressure in old males. Plasma leptin levels were similar in old male and female SHR and in old versus young females. These data suggest that the hypertension in old female SHR is in part due to activation of the sympathetic nervous system, that the renal nerves contribute to the hypertension, and that the mechanism responsible for sympathetic activation in old females is independent of the MC3/4R.

(1976), the California Supreme Court held that mental health providers have an obligation to protect persons who could be harmed by a patient.

No abstract

Background and Hypothesis: The initial assessment of late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMR) reflects cardiac damage and is an important prognostic factor in patients with acute ST-elevation myocardial infarction (STEMI). N-Terminal prohormone of brain natriuretic peptide (NT-proBNP) is released following cardiomyocytes injury. However, the relationship between NT-proBNP levels, myocardial damage and clinical outcomes after STEMI has not been well defined. Methods: Plasma levels of NT-proBNP, troponin I and creatinine kinase (CK) were assessed in 75 patients with STEMI. Echocardiography and CMR were performed prior to hospital discharge. Cardiac damage was quantified using peak biomarker levels and LGE. Patients were followed for a median of 975 days (IQR 823-1098 days) for major adverse cardiac events (MACE) (all-cause mortality, recurrent myocardial infraction, unplanned recurrent revascularization and recurrent hospitalization for heart failure). Results: Plasma levels of NT-proBNP increased following STEMI to peak at 24 hours. The dynamic changes in plasma NT-proBNP were similar to those noted with troponin I and its delayed peak but not those observed with plasma CK levels. Peak NT-proBNP levels correlated positively with indices of myocardial damage such as peak troponin I (R =0.38, P <0.001), peak CK (R =0.22, P = 0.01) and LGE examination (R = 0.46, P <0.001). Peak plasma level of NT-proBNP was strongly predictive of MACE during the follow-up period. Conclusions: Peak levels of NT-proBNP following STEMI are predictive of the extent of myocardial damage and clinical outcomes. These results suggest an important prognostic role for NT-proBNP assessment in STEMI patients.

The Carney complex (CNC) is a rare autosomal dominant genetic complex that is characterised by multiple neoplasms consisting of neuroendocrine and cardiac tumours, with only 750 cases reported worldwide as of 2017. Cardiac tumours, in the context of the CNC, are of unique importance since the leading causes of death in patients with CNC are cardiac. To prevent sudden cardiac death and embolic events, a difficult diagnosis must be made and postdiagnostic screenings must be regular. We present a case of a 52-year-old man, with a medical history of pituitary microadenoma and facial lentiginosis, who presented with dyspnoea 2 months after suffering a cerebrovascular accident.

Pulmonary embolism (PE) is one of the most common causes of cardiovascular (CV) mortality worldwide. Owing to the associated morbidity and mortality with other treatment modalities, including systemic thrombolysis, a discernible change in the era of acute pulmonary embolism management has been reported. Catheter-directed thrombectomy using the FlowTriever system (Inari Medical; Irvine, CA, USA) was shown to reduce endpoints of interest in patients with acute intermediate-high risk PE and was associated with rapid hemodynamic improvement. In this report, we describe our experience with three cases of patients presenting with submassive PE, whereby immediate pulmonary artery pressure improvement was evident in all cases after successful mechanical thrombectomy. Our experience supports the use of FlowTriever mechanical thrombectomy for the treatment of submassive PE in clinical practice, with a call for further research to establish associated benefits.

Background: Heart failure with preserved ejection fraction continues to pose multiple challenges in terms of accurate diagnosis, treatment, and associated morbidity. Accurate left ventricular (LV) mass calculation yields essential prognostic information relating to structural heart disease. Two-dimensional (2D) echocardiography-based calculations are solely limited to LV geometric assumptions of symmetry, whereas three-dimensional (3D) echocardiography could overcome these limitations. This study aims to compare the performance of 2D and 3D LV mass calculations.Methods: A prospective review of echocardiography findings at the University of Louisville, Kentucky, was conducted and assessed. Normal ejection fraction (EF) was defined as >=52% in males and >=54% in females. The following calculations were performed: relative wall thickness (RWT) = 2x posterior wall thickness/LV internal diastolic dimension (LVIDd) and 2D LV mass = 0.8{1.04([LVIDd + IVSd +PWd]3 - LVIDd3)} + 0.6. Concentric hypertrophy was RWT > 0.42 and LV mass >95 kg/m2 in females or > 115 kg/m2 in males. The same cut-offs were used for 2D and 3D echocardiography.Results: Echocardiographic findings for a total number of 154 patients in the study were investigated. There was a weak positive correlation between 2D and 3D LV mass indices (R= 0.534, r2= 0.286, p= 0.001). Seventy patients had 3D EF >=45% with clinical heart failure (HFpEF). Among HFpEF patients, LV hypertrophy (LVH) was present in 74% of patients by 2D echocardiography and 30% by 3D echocardiography (McNemar test p= 0.001). Using 3D echocardiography as the reference, 68% of normal patients were misdiagnosed with LV hypertrophy by 2D echocardiography. Two-thirds of the patients with concentric remodeling by 3D echocardiography were misclassified as having concentric hypertrophy by 2D echocardiography (p=0.001).Conclusion: Adapting necropsy-proven LV mass index cutoffs, 2D over-diagnosed LV hypertrophy through overestimation of the mass, compared to 3D echocardiography. In turn, the majority of HFpEF patients showed no structural hypertrophy of the LV on 3D imaging. This suggests that the majority of patients with HFpEF may qualify for pharmacological prevention to prevent further progression to LV remodeling or LVH.

No abstract