Infective endocarditis in patients who have undergone transcatheter aortic valve implantation: a review.

BACKGROUND: Transcatheter aortic valve implantation (TAVI) has been approved for the treatment of severe aortic stenosis since 2008 and recent trials have shown that TAVI is at least non-inferior to surgical aortic valve replacement (SAVR) with regards to short-term efficacy and safety in patients across all surgical risk profiles. Prosthetic valve endocarditis of the transcatheter heart valve is a feared complication; data on the risk of infective endocarditis (IE) subsequent to TAVI are now gradually emerging. OBJECTIVES: We set forth to conduct a review of the incidence, diagnosis, microbial aetiologies, prevention, outcome and management of TAVI-IE. SOURCES: From the MEDLINE database we included a total of 12 observational studies and five studies of long-term results from randomized controlled trials. CONTENT: The incidence of TAVI-IE was reported to be between 0.7% and 3.0% per person-year. The most common microbes were reported to be enterococci, Staphylococcus aureus, streptococci and coagulase-negative staphylococci. International guidelines on prevention strategies of IE recommend good sanitary conditions including cutaneous care, good oral hygiene and good care of dialysis catheters. Antibiotic prophylaxis is recommended by guidelines prior to dental procedures in patients with TAVI; however, evidence is sparse. The majority of the patients included in this review with TAVI-IE had an indication for surgical intervention due to IE (50.0% or more); however, only a small subset of the patients underwent surgery (16.4% or less). The in-hospital mortality was around 25%, i.e. of the same order of magnitude as in prosthetic valve IE in general, but varied substantially between studies (from 11% to 64%). IMPLICATIONS: The US Food and Drug Administration's approval of TAVI in patients at low surgical risk may change the characteristics of patients with TAVI, which may influence the incidence, management, and outcome of patients with TAVI-IE.

The feasibility of tricuspid annular plane systolic excursion performed by transesophageal echocardiography throughout heart surgery and its interchangeability with transthoracic echocardiography.

Tricuspid annular plane systolic excursion (TAPSE) is a robust measure of RV function, but the performance of transesophageal echocardiography (TEE) measured TAPSE during surgery is not well established. We aim to evaluate feasibility of various TEE views before, during and after surgery. Furthermore, we compare performance of individual TEE measurements depending on view and method (AMM- and M-mode as well as 2D) as well as TAPSE measured using TEE with transthoracic echocardiography (TTE) TAPSE. The study was conducted from January 2015 through September 2016. In 47 patients with normal left ventricular ejection fraction, TEE was prospectively performed during coronary artery bypass grafting surgery. TAPSE and tricuspid annulus tissue Doppler imaging (TDI) were recorded in five different views at pre-specified time points during surgery. Data were analyzed for availability (obtainable/readable images) and reliability (intra-/inter-observer bias and precision). Finally, TEE TAPSE was compared to TTE TAPSE immediately before and after surgery. TAPSE and TDI with TEE was achievable in > 90% of patients in the transgastric view during surgery. The AM- and M-mode had the best reliability and the best correlation with TAPSE measured with TTE. The deep transgastric view was achievable in less than 50% after sternotomy, and TAPSE measured from 2D had a poorer performance compared to the AM- and M-mode. TDI demonstrated a high reliability throughout surgery. RV function can be evaluated by TAPSE and TDI using TEE during surgery. TEE values from the transgastric view demonstrated high performance throughout surgery and a good agreement with TTE TAPSE measurements.

Percutaneous left atrial appendage occlusion for stroke prevention in atrial fibrillation: an update.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia encountered in clinical practice. One of its most devastating complications is the development of thromboembolism leading to fatal or disabling stroke. Oral anticoagulation (OAC, warfarin) is the standard treatment for stroke prevention in patients with AF with an increased stroke risk. However, there are several obstacles to long-term OAC therapy, including the risk of serious bleeding, several drug-drug interactions and the need for frequent blood testing. Although newer oral anticoagulants have been developed, these drugs also face issues of major bleeding and non-compliance. Therefore, alternative treatment options for stroke prevention in patients with AF with a high stroke risk are needed. Percutaneous left atrial appendage (LAA) occlusion is an evolving therapy, which should be taken into consideration in those patients with non-valvular AF with a high stroke risk and contraindications for OAC. This article aims to discuss the rationale for LAA closure, the available LAA occlusion devices and their clinical evidence until now. Moreover, we discuss the importance of proper patient selection, the role of various imaging techniques and the need for a more tailored postprocedural antithrombotic therapy.

Effects of acute and chronic attenuation of postprandial hyperglycemia on postglucose-load endothelial function in insulin resistant individuals: is stimulation of first phase insulin secretion beneficial for the endothelial function?

The aim of the study is to determine if attenuation of postprandial hyperglycemia, by acutely and chronically enhancing postprandial insulin secretion in insulin-resistant individuals, improves the endothelial dysfunction. We assessed postoral glucose-load endothelial function in 56 insulin-resistant subjects with the Flow-Mediated-Dilation (FMD) technique. We randomized subjects to intervention/control group, and examined the acute and chronic effect of nateglinide, an oral antidiabetic drug of rapid action. In the intervention group, postoral glucose-load (post-OGL) FMD delta values deteriorated when compared to pre-OGL values, most significantly at 3 h post-OGL, on the following days: on the first study day termed "Baseline day" (p=0.04); on both days after 3 months of nateglinide treatment [with nateglinide administered on study-day "acute+chronic" (p=0.01); and without nateglinide on study-day "Closing day", p=0.001]. Post-OGL changes in the control group were nonsignificant both at Baseline and on Closing day. After a single dose of nateglinide "Acute day", post-OGL FMD deterioration was abolished. There was an increment in post-OGL FMD delta values most significant at 2 h post-OGL (p=0.02). Insulin concentrations increased while glucose concentrations decreased on study-days with nateglinide when compared to study-days without (p=<0.001 for both insulin and glucose). Comparisons for insulin and glucose concentrations between days with nateglinide, and likewise between days without, showed no significant difference. Postglucose load endothelial dysfunction can be prevented by administration of nateglinide, however, after 3 months of nateglinide treatment, this effect is abolished. Chronically increased insulin secretion could counteract the initial beneficial effect of reduced glucose excursions. We found no relationship between postprandial hyperglycemia and post-OGL FMD.

Effects of oral glucose load on endothelial function and on insulin and glucose fluctuations in healthy individuals.

BACKGROUND/AIMS: Postprandial hyperglycemia, an independent risk factor for cardiovascular disease, is accompanied by endothelial dysfunction. We studied the effect of oral glucose load on insulin and glucose fluctuations, and on postprandial endothelial function in healthy individuals in order to better understand and cope with the postprandial state in insulin resistant individuals. METHODS: We assessed post-oral glucose load endothelial function (flow mediated dilation), plasma insulin, and blood glucose in 9 healthy subjects. RESULTS: The largest increases in delta FMD values (fasting FMD value subtracted from postprandial FMD value) occurred at 3 hours after both glucose or placebo load, respectively: 4.80 +/- 1.41 (P = .009) and 2.34 +/- 1.47 (P = .15). Glucose and insulin concentrations achieved maximum peaks at one hour post-glucose load. CONCLUSION: Oral glucose load does not induce endothelial dysfunction in healthy individuals with mean insulin and glucose values of 5.6 mmol/L and 27.2 mmol/L, respectively, 2 hours after glucose load.

Normal insulin-stimulated endothelial function and impaired insulin-stimulated muscle glucose uptake in young adults with low birth weight.

Low birth weight has been linked to insulin resistance and cardiovascular disease. We hypothesized that insulin sensitivity of both muscle and vascular tissues were impaired in young men with low birth weight. Blood flow was measured by venous occlusion plethysmography during dose-response studies of acetylcholine and sodium nitroprusside in the forearm of fourteen 21-yr-old men with low birth weight and 16 controls of normal birth weight. Glucose uptake was measured during intraarterial insulin infusion. Dose-response studies were repeated during insulin infusion. The maximal blood flow during acetylcholine infusion was 14.1 +/- 2.7 and 14.4 +/- 2.1 [ml x (100 ml forearm)(-1) x min(-1)] in low and normal birth weight subjects, respectively. Insulin coinfusion increased acetylcholine-stimulated flow in both groups: 18.0 +/- 3.1 vs. 17.9 +/- 3.1 [ml x (100 ml forearm)(-1) x min(-1)], NS. Insulin infusion increased glucose uptake significantly in the normal birth weight group, compared with the low birth weight group: 0.40 +/- 0.09 to 1.00 +/- 0.16 vs. 0.44 +/- 0.09 to 0.59 +/- 0.1 [ micro mol glucose x (100 ml forearm)(-1) x min(-1)], P = 0.04. Young men with low birth weight have normal insulin-stimulated endothelial function and impaired insulin-stimulated forearm glucose uptake. Thus, endothelial dysfunction does not necessarily coexist with metabolic alterations in subjects with low birth weight.

Impaired vascular reactivity is present despite normal levels of von Willebrand factor in patients with uncomplicated Type 2 diabetes.

BACKGROUND: Type 2 diabetes is associated with an increased risk of cardiovascular disease. Endothelial dysfunction is thought to be an early marker of atherosclerosis. The purpose of this study was to assess whether endothelial function, judged by measurements of flow-mediated vasodilatation (FMD) and nitroglycerine (NTG)-induced vasodilatation as well as serum levels of von Willebrand factor, was affected in patients with uncomplicated Type 2 diabetes and normal levels of urinary albumin excretion (UAE). SUBJECTS AND METHODS: Twenty-three patients with Type 2 diabetes, normal UAE and no vascular complications were examined. Twenty-three healthy subjects matched for age, gender, body mass index and resting vessel size served as controls. All participants were non-smokers. Endothelial function was assessed by high-resolution ultrasound which measures changes in diameter of the brachial artery during flow-mediated and NTG-induced vasodilatation. We also measured serum levels of von Willebrand factor. RESULTS: In Type 2 diabetic patients FMD (3.2 +/- 0.5% vs. 4.8 +/- 0.5%, P = 0.019) as well as NTG-induced vasodilatation (15.9 +/- 0.6% vs. 18.5 +/- 0.9%, P = 0.021) were significantly reduced compared with controls. Levels of von Willebrand factor were not different between groups (0.88 +/- 0.07 vs. 0.88 +/- 0.07 in patients and controls, respectively) and were not correlated to FMD or NTG-induced vasodilatation. CONCLUSION: Impaired vascular reactivity is present in uncomplicated Type 2 diabetes and seems to be a more sensitive marker of vascular dysfunction than von Willebrand factor.

Insulin therapy improves insulin-stimulated endothelial function in patients with type 2 diabetes and ischemic heart disease.

Blunted insulin-stimulated endothelial function may be a mechanism for the development of atherothrombotic disease in type 2 diabetes, but it is unknown whether hypoglycemic drug therapy can modulate this abnormality. We studied patients with type 2 diabetes and stable ischemic heart disease (n = 28) and lean, healthy control subjects (n = 31). Forearm blood flow was measured by venous occlusion plethysmography during dose-response studies of acetylcholine (ACh) and sodium nitroprusside (SNP) infused into the brachial artery. In the patients and 10 healthy control subjects, ACh was repeated after intrabrachial infusion of insulin. Patients were restudied after 2 months of insulin therapy with four daily subcutaneous injections (treatment group, n = 19) or without hypoglycemic drug therapy (time control group, n = 9). Insulin infusion raised venous serum insulin in the forearm to high physiological levels (133 +/- 14.6 mU/l in patients) with a minor increase in systemic venous serum insulin. This increased the ACh response by 149 +/- 47, 110 +/- 33, 100 +/- 45, and 106 +/- 44% during the four ACh doses in healthy control subjects (P < 0.0001) but had no effect in patients (P = 0.3). After 2 months, HbA(1c) in the treatment group had decreased from 10.0 +/- 0.4 to 7.5 +/- 0.2%. Although neither the ACh response (P = 0.09) nor the SNP response (P = 0.4) had changed significantly, insulin stimulation had a significant effect, as the ACh response increased by 58 +/- 25, 84 +/- 66, 120 +/- 93, and 69 +/- 36% (P = 0.0002). In the time control group, insulin stimulation remained without effect after 8 weeks (P = 0.7). In conclusion, insulin therapy partly restores insulin-stimulated endothelial function in patients with type 2 diabetes and ischemic heart disease.

Circulating immunoreactive proANP1-30 and proANP31-67 responses to acute exercise.

The circulating immunoreactive atrial natriuretic peptide (C-terminal; alpha-ANP) increases during exercise to become suppressed in the first hours of the recovery. The response of the N-terminal ANP fragments to acute exercise is not known while proANP (31-67) appears to be elevated with chronic exercise. We evaluated the plasma concentrations of the N-terminal ANP fragments (1-30) and (31-67) in oarsmen (n=10) before and after two acute exercise bouts separated by 5 h. As control, measurements were made on a day with no exercise (n=12). At rest, the concentrations of proANP(1-30) and proANP(31-67) were 344+/-42 and 810+/-172 pmol x l(-1), respectively. Half an hour after the first exercise bout, proANP(1-30) was elevated (to 404+/-48 pmol x l(-1); P<0.05) and decreased below the pre-exercise level (to 316+/-41 pmol x l(-1); P<0.05) 4 h into the recovery period. Also, 30 min after the second exercise session, the concentration of proANP(1-30) was elevated to 408+/-45 pmol x l(-1) (P<0.05) and the pre-exercise level was re-established on the following morning. Thus, proANP(1-30), rather than proANP(31-67), responded to acute exercise. These results suggest that atrial distension and, therefore, the central blood volume changes markedly in athletes during a day with repeated exercise bouts.