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Antti Saraste

Bio: Antti Saraste is an academic researcher from Turku University Hospital. The author has contributed to research in topics: Coronary artery disease & Medicine. The author has an hindex of 43, co-authored 255 publications receiving 11508 citations. Previous affiliations of Antti Saraste include University of Turku & VU University Medical Center.


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Journal ArticleDOI
TL;DR: In this article, the authors present guidelines for the management of patients with coronary artery disease (CAD), which is a pathological process characterized by atherosclerotic plaque accumulation in the epicardial arteries.
Abstract: Coronary artery disease (CAD) is a pathological process characterized by atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or non-obstructive. This process can be modified by lifestyle adjustments, pharmacological therapies, and invasive interventions designed to achieve disease stabilization or regression. The disease can have long, stable periods but can also become unstable at any time, typically due to an acute atherothrombotic event caused by plaque rupture or erosion. However, the disease is chronic, most often progressive, and hence serious, even in clinically apparently silent periods. The dynamic nature of the CAD process results in various clinical presentations, which can be conveniently categorized as either acute coronary syndromes (ACS) or chronic coronary syndromes (CCS). The Guidelines presented here refer to the management of patients with CCS. The natural history of CCS is illustrated in Figure 1.

3,448 citations

Journal ArticleDOI
TL;DR: Clinicians will find the recommendations in these revised CPGs useful in their daily work and can be reassured that the recommendations have been vetted thoroughly by the most rigorous scientific process, so that cardiovascular clinicians worldwide may deliver optimal, standardized care.
Abstract: AAA : abdominal aortic aneurysm ACEI : angiotensin converting enzyme inhibitor ACS : acute coronary syndromes AF : atrial fibrillation AKI : acute kidney injury AKIN : Acute Kidney Injury Network ARB : angiotensin receptor blocker ASA : American Society of Anesthesiologists b.i.d. : bis in diem (twice daily) BBSA : Beta-Blocker in Spinal Anesthesia BMS : bare-metal stent BNP : B-type natriuretic peptide bpm : beats per minute CABG : coronary artery bypass graft CAD : coronary artery disease CARP : Coronary Artery Revascularization Prophylaxis CAS : carotid artery stenting CASS : Coronary Artery Surgery Study CEA : carotid endarterectomy CHA2DS2-VASc : cardiac failure, hypertension, age ≥75 (doubled), diabetes, stroke (doubled)-vascular disease, age 65–74 and sex category (female) CI : confidence interval CI-AKI : contrast-induced acute kidney injury CKD : chronic kidney disease CKD-EPI : Chronic Kidney Disease Epidemiology Collaboration Cmax : maximum concentration CMR : cardiovascular magnetic resonance COPD : chronic obstructive pulmonary disease CPG : Committee for Practice Guidelines CPX/CPET : cardiopulmonary exercise test CRP : C-reactive protein CRT : cardiac resynchronization therapy CRT-D : cardiac resynchronization therapy defibrillator CT : computed tomography cTnI : cardiac troponin I cTnT : cardiac troponin T CVD : cardiovascular disease CYP3a4 : cytochrome P3a4 enzyme DAPT : dual anti-platelet therapy DECREASE : Dutch Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography DES : drug-eluting stent DIPOM : DIabetic Post-Operative Mortality and Morbidity DSE : dobutamine stress echocardiography ECG : electrocardiography/electrocardiographically/electrocardiogram eGFR : estimated glomerular filtration rate ESA : European Society of Anaesthesiology ESC : European Society of Cardiology EVAR : endovascular abdominal aortic aneurysm repair FEV1 : Forced expiratory volume in 1 second HbA1c : glycosylated haemoglobin HF-PEF : heart failure with preserved left ventricular ejection fraction HF-REF : heart failure with reduced left ventricular ejection fraction ICD : implantable cardioverter defibrillator ICU : intensive care unit IHD : ischaemic heart disease INR : international normalized ratio IOCM : iso-osmolar contrast medium KDIGO : Kidney Disease: Improving Global Outcomes LMWH : low molecular weight heparin LOCM : low-osmolar contrast medium LV : left ventricular LVEF : left ventricular ejection fraction MaVS : Metoprolol after Vascular Surgery MDRD : Modification of Diet in Renal Disease MET : metabolic equivalent MRI : magnetic resonance imaging NHS : National Health Service NOAC : non-vitamin K oral anticoagulant NSQIP : National Surgical Quality Improvement Program NSTE-ACS : non-ST-elevation acute coronary syndromes NT-proBNP : N-terminal pro-BNP O2 : oxygen OHS : obesity hypoventilation syndrome OR : odds ratio P gp : platelet glycoprotein PAC : pulmonary artery catheter PAD : peripheral artery disease PAH : pulmonary artery hypertension PCC : prothrombin complex concentrate PCI : percutaneous coronary intervention POBBLE : Peri-Operative Beta-BLockadE POISE : Peri-Operative ISchemic Evaluation POISE-2 : Peri-Operative ISchemic Evaluation 2 q.d. : quaque die (once daily) RIFLE : Risk, Injury, Failure, Loss, End-stage renal disease SPECT : single photon emission computed tomography SVT : supraventricular tachycardia SYNTAX : Synergy between Percutaneous Coronary Intervention with TAXUS and Cardiac Surgery TAVI : transcatheter aortic valve implantation TdP : torsades de pointes TIA : transient ischaemic attack TOE : transoesophageal echocardiography TOD : transoesophageal doppler TTE : transthoracic echocardiography UFH : unfractionated heparin VATS : video-assisted thoracic surgery VHD : valvular heart disease VISION : Vascular Events In Noncardiac Surgery Patients Cohort Evaluation VKA : vitamin K antagonist VPB : ventricular premature beat VT : ventricular tachycardia Guidelines summarize and evaluate all available evidence, at the time of the writing process, on a particular issue with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic …

1,353 citations

Journal ArticleDOI
TL;DR: A review of the molecular mechanisms of apoptosis as they relate to the morphologic hallmarks and their implications for the detection of cancer cell apoptosis in cardiac tissue is presented in this article.
Abstract: Apoptosis is characterised by a series of typical morphological features, such as shrinkage of the cell, fragmentation into membrane-bound apoptotic bodies and rapid phagocytosis by neighbouring cells. This paper reviews the current knowledge on the molecular mechanisms of apoptosis as they relate to the morphologic hallmarks and their implications for the detection of apoptosis in cardiac tissue. Activation of cysteine proteases called caspases plays a major role in the execution of apoptosis. These proteases selectively cleave vital cellular substrates, which results in apoptotic morphology and internucleosomal fragmentation of DNA by selectively activated DNases. In response to several pro-apoptotic signals, mitochondria release caspase activating factors, that initiate an escalating caspase cascade and commit the cell to die. Members of the Bcl-2 oncoprotein family control mitochondrial events and are able to prevent, or induce, both apoptotic and non-apoptotic types of cell death. This suggests that different types of cell death share common mechanisms in the early phases, whereas activation of caspases determines the phenotype of cell death. Detection of apoptotic cells in tissue samples currently relies on the TUNEL assay. TUNEL-positive cardiomyocytes show morphological features of apoptosis and the typical ladder pattern in DNA electrophoresis. Thus, provided that the staining protocol is carefully standardised, this quantitative methodology provides reproducible results of the occurrence of cardiomyocyte apoptosis in cardiac samples. Recently, potentially more specific assays based on analysis of DNA fragmentation or demonstration of caspase activation have been developed. Applicability of these assays to demonstrate cardiomyocyte apoptosis should be tested.

1,319 citations

Journal ArticleDOI
TL;DR: This study provides evidence that in addition to overt necrosis, a subset of myocytes undergo apoptosis during ischemia-reperfusion injury and may provide a new target for cardioprotection during evolving AMI in humans.
Abstract: Background After reopening of the infarct-related coronary artery, cardiomyocytes continue to die during reperfusion. The mechanisms of cell death have been subject to debate. We studied whether an apoptotic type of cell death occurs in human acute myocardial infarction (AMI). Methods and Results We studied myocardial samples of eight patients who died of AMI and had patent infarct-related arteries at autopsy. Six of the patients had received initially successful thrombolysis. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the in situ DNA end-labeling method. Apoptotic cardiomyocytes were observed particularly in the border zones of histologically infarcted myocardium, whereas very few apoptotic cells were present in the remote noninfarcted myocardium. Internucleosomal fragmentation was confirmed by agarose gel electrophoresis of DNA isolated from the representative myocardial areas. Conclusions This study provides evidence that in addi...

792 citations


Cited by
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TL;DR: Authors/Task Force Members: Piotr Ponikowski* (Chairperson) (Poland), Adriaan A. Voors* (Co-Chair person) (The Netherlands), Stefan D. Anker (Germany), Héctor Bueno (Spain), John G. F. Cleland (UK), Andrew J. S. Coats (UK)

13,400 citations

Journal ArticleDOI
19 May 2011-Nature
TL;DR: Preclinical and clinical studies have shown new molecular targets and principles, which may provide avenues for improving the therapeutic benefit from anti-angiogenic strategies.
Abstract: Blood vessels deliver oxygen and nutrients to every part of the body, but also nourish diseases such as cancer. Over the past decade, our understanding of the molecular mechanisms of angiogenesis (blood vessel growth) has increased at an explosive rate and has led to the approval of anti-angiogenic drugs for cancer and eye diseases. So far, hundreds of thousands of patients have benefited from blockers of the angiogenic protein vascular endothelial growth factor, but limited efficacy and resistance remain outstanding problems. Recent preclinical and clinical studies have shown new molecular targets and principles, which may provide avenues for improving the therapeutic benefit from anti-angiogenic strategies.

4,441 citations