Recommendations for driving after implantable cardioverter defibrillator implantation and the use of a wearable cardioverter defibrillator : Different viewpoints around the world.

The use of implantable cardioverter defibrillators (ICD) has been shown to improve survival in patients at risk of sudden cardiac death; however, due to the continuous risk of sudden loss of consciousness during arrhythmia or ICD intervention, they pose a potential risk to other road users while driving. A large number of opinions and recommendations from authorities and medical societies all over the world exist regarding driving restrictions after ICD implantation. This analysis provides an overview of the recommendations on driving restrictions from several countries. Furthermore, the use of the wearable and the subcutaneous ICD are taken into account.

Lipoprotein apheresis - Shortening of treatment intervals reduces cardiovascular events: Case reports.

BACKGROUND: Lipoprotein (Lp-) apheresis is a life-long therapy, usually performed in weekly intervals. In some cases, however, atherosclerotic disease progresses despite adequate therapy with weekly Lp-apheresis and maximal lipid lowering medication. In an attempt to improve the effectiveness of therapy, we temporarily shortened treatment intervals of Lp-apheresis in patients with elevated lipoprotein(a) (Lp(a)) and further progression of coronary atherosclerosis despite weekly Lp-apheresis and maximal lipid lowering medication. METHODS: We illustrate three case reports of patients with elevated Lp(a), who underwent regular weekly Lp-apheresis treatment for secondary prevention. The intensified treatment protocol contained three therapies in two weeks (alternating 2 per week and 1 per week). RESULTS: The shortening of treatment intervals achieved a stabilization of atherosclerotic disease in case 1. After a total of 68 therapies in 52 weeks (1.31 sessions/week) the elective coronary angiography revealed excellent long-term results. In case 2, the intensified treatment protocol is still ongoing. The patient reported a decrease in angina pectoris and an increase in exercise capacity since the beginning of more frequent therapy sessions. In some cases, as it is shown in case 3, a fast decision for shortening the treatment intervals is necessary. CONCLUSIONS: The intensified treatment regimen resulted in an improvement in clinical symptoms and no further progression of atherosclerosis. In conclusion, shorter therapeutic Lp-apheresis intervals, at least temporarily, should be considered in patients who suffer from clinical and/or angiographic progression of atherosclerosis, despite maximal lipid lowering medication and weekly Lp-apheresis.

One year follow-up of patients with reduced left ventricular ejection fraction (LVEF) on lipoprotein apheresis.

BACKGROUND: Left ventricular ejection fraction (LVEF) is a valuable measure to assess left ventricular systolic function. Lipid lowering therapy by statins has been shown to have an impact on LVEF already after a 6 months treatment. Higher doses of statins have been claimed to be more effective as compared to a conventional one and even a difference between lipophilic and hydrophilic compounds has been reported. The effect of regular lipoprotein-apheresis (LP-apheresis) on LVEF was previously poorly examined. Patients involved in a regular LP-apheresis program are supposed to undergo a number of follow-up investigations among them myocardial scintigraphy and LVEF, measured by radionuclide ventriculography. METHODS: We examined 18 patients before initiation and after one year of ongoing LP-apheresis. 13 patients (11 males, 2 females, mean age 58.3 ±â€¯5.3 years, groups A) were since more than a year on stable, unchanged statin treatment (atorvastatin 40 mg, simvastatin 40 mg, rosuvastatin 20 mg±ezetimibe), the other 5 patients (3 males, 2 females, mean age 57.1 ±â€¯4.6 years, group B) were intolerant to statins being on micronized fenofibrate±resorption inhibitors (cholestyramine). All patients had a Lp(a) < 30 mg/dl. As part of the usual follow-up monitoring, LVEF was determined by means of radionuclide ventriculography after application of 550 MBq 99m Tc-pertechnetate. RESULTS: The follow-up LVEF was checked at a mean of 48.7 weeks in group A and 51.2 weeks in group B. Except in 1 patient (LVEF 46.8% before vs. 45.2% after LP-apheresis initiation) in group A we noted a significant increase in LVEF in 12 patients of group A (92%) and in all patients of group B. Mean LVEF increased significantly in both groups (A: 42.7±8.1 → 46.5±7.5% (p < 0.001) and B: 41.9±8.4 → 46.5±6.3 %; p < 0.001). The relative rise was nearly identical (group A 9.6%, in group B 9.7%). CONCLUSIONS: Our findings indicate that regular long-term LP-apheresis treatment apparently increases LVEF, independently on current statin treatment. This implies a role of lowering of atherogenic lipoproteins as underlying mechanism. A prospective study should clarify the relative extent of LVEF improvement induced by LP-apheresis.

Lipoprotein apheresis in Austria - Reduction of cardiovascular events by regular lipoprotein apheresis treatment.

BACKGROUND: In Austria, about 12 patients per 1 million inhabitants are treated currently with lipoprotein (LP-) apheresis. In 2016 it has been suggested, that about 5000 patients were treated worldwide with LP-apheresis, more than half of them in Germany. Regular LP-apheresis aims to decrease apolipoprotein B-rich lipoproteins and to reduce cardiovascular events. In this analysis we present the current situation of LP-apheresis in Austria and we evaluated the cardiovascular event rate 2 years before versus 2 years after starting LP-apheresis. METHODS: A retrospective analysis of 30 patients (19 men and 11 women) was performed at Athos Institute, Vienna, Austria. The study period included two years prior versus two years after the beginning of LP-apheresis. Cardiovascular events and interventions were defined as regarding the coronary (MACE) or the non-coronary (peripheral, cerebral or renal) vascular system. RESULTS: The first cardiovascular event before treatment initiation occurred at a mean age of 48.4 years (range 34-73), treatment was started at a mean age of 55.6 years (range 34-73). The mean rate of incidence of cardiovascular events per patient per 2 years before beginning of LP-apheresis (y-2 and y-1) versus 2 years during treatment (y+1 and y+2) was reduced by 77.78% (1.50 versus 0.33 events/patient/2 years, p = 0.003). CONCLUSIONS: The significant reduction in MACE and vascular disease during regular LP-apheresis at weekly intervals is consistent with data from the literature. Difficulties arise in comparing such studies due to different definition of events or interventions and different study durations. However, LP-apheresis is an efficient treatment option and causes significantly prolonged event-free survival for patients at risk.

Statin-induced muscular side effects at rest and exercise - An anatomical mapping.

BACKGROUND AND AIMS: Muscle-related symptoms with or without creatine kinase (CK) elevation are common adverse effects associated with statin use. Symptoms are ranging from benign myalgia to myositis and in rare cases to rhabdomyolysis. The aim was to characterize and describe muscular side effects and create an anatomical frequency mapping. METHODS: The prospective observational study was performed at a large lipidology outpatient unit in Vienna. 1111 consecutively admitted patients with muscular side effects on statin monotherapy were included during a 4-year period. Anatomical mapping of the affected muscles, signs and symptoms, the onset of symptoms after starting statin therapy and disappearance after cessation of treatment was assessed. RESULTS: In 96.5% of the patients with muscle symptoms, there was no elevation of CK. The anatomical mapping revealed exercised muscles as being mainly affected in 84%. In the upper extremity, symptoms were mainly described at the dominating side. Mostly affected muscles were the pectoral (61.4%), followed by the quadriceps femoris (59.8%), the biceps brachii (54.3%) and the deltoid (22.5%) muscles. The majority of symptoms (76.9%, n = 854) appeared within 29 days. Symptoms disappeared after discontinuation of statin therapy at a mean of 5.4 days. CONCLUSIONS: Physical activity seems to be a key trigger for onset of statin-induced muscular side effects. The appearance of symptoms can be symmetrical, asymmetrical, generalized or in isolated muscle groups only. Different statins usually produce similar symptoms, but often some patients tolerate one statin better than another.

Alirocumab as add-on therapy to statins: current evidence and clinical potential.

Atherosclerotic cardiovascular diseases (ASCVDs) are associated with a substantial mortality, physical morbidity, and mental disability. Elevated plasma low-density lipoprotein cholesterol (LDL-C) levels play a major role in the pathophysiology of ASCVDs. Statins have been shown to reduce ASCVD risk and associated events and are recommended as first-line therapy for treatment of hypercholesterolemia by current international guidelines. The key issue is to attain guideline-recommended LDL-C levels (below 70 mg/dl) for patients at very high cardiovascular risk. However, many high-risk and very-high-risk patients on statin therapy remain beyond treatment goals despite lifestyle modification and statins, and are exposed to a high risk of future cardiovascular events including myocardial infarction (MI), stroke, revascularization procedures, and death. This clearly emphasizes the urgent need for additional LDL-C reduction with new therapeutic strategies to target these highly atherogenic particles and to further reduce the burden of ASCVDs. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a major role as a key regulator of the hepatic LDL receptor recycling process. Developments over the past 15 years have demonstrated PCSK9 inhibition to be a novel therapeutic strategy to manage increased LDL-C levels. A number of clinical studies using humanized monoclonal antibody technology against PCSK9 have shown profound reductions of LDL-C levels when used either alone or in combination with statin therapy. Recently, the first cardiovascular outcome study demonstrated a significant reduction of ASCV events when evolocumab was added to a statin therapy. This review will discuss current knowledge about antibody-mediated PCSK9 inhibition as add-on therapy to statin and the clinical potential that may be expected.

[Therapeutic options in hyperlipidemia]. / Therapieoptionen von Fettstoffwechselstörungen.

Treatment of lipid disorders (dyslipidemia) is the cornerstone of atherosclerosis prevention and reduction of progression. Lifestyle modification is the first step to improve the plasma lipid profile. Statins play a central role in the reduction of LDL cholesterol. Whether and to what extent other lipids such as triglycerides or lipoprotein(a) should also be treated depends on the extent of atherosclerotic disease and its progression over time. Especially in residential cardiac rehabilitation we have the opportunity to encourage adherence and adapt medication as necessary due to a face to face contact over 4 weeks. Moreover, the prescription for a PCSK9-inhibitor could be resolved or the indication for a lipoprotein apheresis could be considered.

Acute Severe Mitral Stenosis Immediately After Transcatheter Aortic Valve Implantation.

An 86-year-old female patient was referred for treatment of symptomatic severe aortic stenosis. The heart team decided to perform transfemoral transcatheter aortic valve implantation. A 25 mm transcatheter aortic valve was implanted, but the valve migrated low into the left ventricular outflow tract. The subsequent removal and replacement procedures are described.

Molecular imaging of atherosclerotic lesions by positron emission tomography - can it meet the expectations?

Early non-invasive imaging of atherosclerosis and in particular the detection of lesions at risk with high specificity could significantly affect cardiovascular morbidity and mortality. Conventional nuclear medicine approaches, in particular using autologous radiolabeled lipoproteins, can be related to histopathological findings; however, they fail to identify lesions at risk. Positron emission tomography (PET) tracers with much better physical properties have been examined, the most detailed information being available for F-18-deoxyglucose (FDG) and F-18-sodium fluoride (NaF). These two approaches are sensitive to different biochemical mechanisms, i.e. inflammation and microcalcification. Initial enthusiasm, in particular for F-18-FDG, has disappeared, although for F-18-NaF there is some hope, but this is not a breakthrough. No tracer is available so far that is able to identify a specific characteristic of a lesion prone to rupture. Other PET tracers in the pipeline have been examined, mainly in experimental models and only a few in patients, but they failed to contribute significantly to early lesion discovery and do not support great expectations. The key question is: Do we understand what we see? Moreover, methodological problems, a lack of standardization of imaging protocols and aspects of quantification provide a wide range for potential future improvements. While monitoring a therapeutic intervention seems to be possible for both F-18-FDG and F-18-NaF, highly specific early identification of lesions at risk by PET imaging is still far away. As of today, PET is not ready for routine clinical judgment of atherosclerotic lesions at risk to rupture. Even if all these problems can be solved, radiation exposure will still remain a concern, in particular for repeated studies.