Macro- and microvascular reactivity during repetitive exposure to shortened sleep: sex differences.

Epidemiological studies have reported strong association between sleep loss and hypertension with unknown mechanisms. This study investigated macrovascular and microcirculation changes and inflammatory markers during repetitive sleep restriction. Sex differences were also explored.

Repetitive exposure to shortened sleep leads to blunted sleep-associated blood pressure dipping.

Background: Blood pressure (BP) dips at night during sleep in healthy individuals but in disturbed sleep, dipping is blunted. However, the impact of chronic insufficient sleep duration, with limited intermittent recovery sleep, on BP dipping is not known. The objective of this study was to examine, in a controlled experimental model, the influence of chronic sleep restriction on BP patterns at night and during the day.

Longitudinal systolic strain, cardiac function improvement, and survival following treatment of light-chain (AL) cardiac amyloidosis.

Aims: To determine whether echocardiographic longitudinal systolic strain (LS) parameters identify short-term improvement following chemotherapy for light-chain (AL) cardiac amyloidosis (CA). Among patients with CA, standard echocardiographic measures are commonly unchanged at 1 year following successful chemotherapy, despite observed reductions in cardiac biomarkers.

Methods And Results: We retrospectively identified 61 patients with AL-CA treated with high-dose melphalan or bortezomib-based regimens.

Increasing sleep duration to lower beat-to-beat blood pressure: a pilot study.

Strong evidence has accumulated over the last several years, showing that low sleep quantity and/or quality plays an important role in the elevation of blood pressure. We hypothesized that increasing sleep duration serves as an effective behavioral strategy to reduce blood pressure in prehypertension or type 1 hypertension. Twenty-two participants with prehypertension or stage 1 hypertension, and habitual sleep durations of 7 h or less, participated in a 6-week intervention study.

Sleep, inflammation and cardiovascular disease.

In data from prospective cohort studies, self report of insufficient or disturbed sleep is related to increased overall and cardiovascular morbidity. Inflammation is established as a key mechanism in the development of arteriosclerotic heart and vascular disease. Inflammation has been considered a possible link between short sleep and cardiovascular disease and morbidity.

Cardiac amyloidosis: evolving approach to diagnosis and management.

The systemic amyloidoses are a group of heterogeneous disorders characterized by extracellular deposition of misfolded fibrillar protein that results in organ dysfunction. Involvement of the heart (cardiac amyloidosis) is manifest by increased cardiac wall thickness and impairment of myocardial diastolic and systolic properties, changes that result in heart failure, dysrhythmia, and death. Amyloidosis is classified by precursor protein, with light-chain (AL) and transthyretin (TTR) disease being most common in the United States.

Outcome of AL amyloidosis after high-dose melphalan and autologous stem cell transplantation: long-term results in a series of 421 patients.

Previous studies have suggested that, in patients with AL amyloidosis treated with high-dose melphalan and autologous stem-cell transplantation (HDM/SCT), the greatest benefit is seen in those patients achieving a hematologic complete response (CR). We analyzed a series of 421 consecutive patients treated with HDM/SCT at a single referral center and compared outcomes for patients with and without CR. Treatment-related mortality was 11.

Sleep loss and inflammation.

Controlled, experimental studies on the effects of acute sleep loss in humans have shown that mediators of inflammation are altered by sleep loss. Elevations in these mediators have been found to occur in healthy, rigorously screened individuals undergoing experimental vigils of more than 24h, and have also been seen in response to various durations of sleep restricted to between 25 and 50% of a normal 8h sleep amount. While these altered profiles represent small changes, such sub-clinical shifts in basal inflammatory cytokines are known to be associated with the future development of metabolic syndrome disease in healthy, asymptomatic individuals.

Matrix metalloproteinases and their tissue inhibitors in cardiac amyloidosis: relationship to structural, functional myocardial changes and to light chain amyloid deposition.

Background: Cardiac amyloidosis is characterized by amyloid infiltration resulting in extracellular matrix disruption. Amyloid cardiomyopathy due to immunoglobulin light chain protein (AL-CMP) deposition has an accelerated clinical course and a worse prognosis compared with non-light chain cardiac amyloidoses (ie, forms associated with wild-type or mutated transthyretin [TTR]). We therefore tested the hypothesis that determinants of proteolytic activity of the extracellular matrix, the matrix metalloproteinases (MMPs), and their tissue inhibitors (TIMPs) would have distinct patterns and contribute to the pathogenesis of AL-CMP versus TTR-related amyloidosis.

Cardiovascular, inflammatory, and metabolic consequences of sleep deprivation.

That insufficient sleep is associated with poor attention and performance deficits is becoming widely recognized. Fewer people are aware that chronic sleep complaints in epidemiologic studies have also been associated with an increase in overall mortality and morbidity. This article summarizes findings of known effects of insufficient sleep on cardiovascular risk factors including blood pressure, glucose metabolism, hormonal regulation, and inflammation with particular emphasis on experimental sleep loss, using models of total and partial sleep deprivation, in healthy individuals who normally sleep in the range of 7 to 8 hours and have no sleep disorders.

Effect of sleep loss on C-reactive protein, an inflammatory marker of cardiovascular risk.

Objectives: We sought to investigate the effects of sleep loss on high-sensitivity C-reactive protein (CRP) levels.

Background: Concentrations of high-sensitivity CRP are predictive of future cardiovascular morbidity. In epidemiologic studies, short sleep duration and sleep complaints have also been associated with increased cardiovascular morbidity.

Endocardial pacemaker or defibrillator leads with infected vegetations: a single-center experience and consequences of transvenous extraction.

Background: Removal of infected endovascular leads if often required for cure of systemic infection, but the perceived risk of embolic events in the presence of large (>10 mm) vegetations has been considered a relative contraindication to transvenous removal. Surgical removal of pacemaker leads has been suggested in this situation to avoid occurrence of pulmonary embolization.

Methods: Of 38 patients with infection of implanted pacemaker or cardioverter-defibrillator devices, those with evidence for systemic infection underwent transesophageal echocardiography to assess for the presence of vegetations.

Paradoxical embolism in the left main coronary artery: diagnosis by transesophageal echocardiography.

We describe a patient with a paradoxical coronary embolism diagnosed by transesophageal echocardiography. The patient developed a stroke followed by a myocardial infarction. Coronary angiography showed an obstruction of the left main coronary artery.

Targeting the use of glycoprotein IIb/IIIa antagonists--the diabetic patient.

Diabetes mellitus is associated with an increased prevalence of and morbidity from coronary artery disease, which is present in at least 25% of diabetic patients. Diabetes mellitus is a risk factor for recurrent cardiovascular events after myocardial infarction and after percutaneous coronary intervention procedures or coronary artery bypass surgery. Less than half of the increase in cardiovascular events with diabetes mellitus is accounted for by the presence of traditional cardiac risk factors such as hypertension, hypercholesterolemia, and hypertriglyceridemia.