Author
Antti Saraste
Other affiliations: University of Turku, VU University Medical Center, University of New South Wales
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.
Papers published on a yearly basis
Papers
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Turku University Hospital1, National University of Ireland, Galway2, University of Catania3, University of Naples Federico II4, University of Paris5, Bispebjerg Hospital6, University of Sheffield7, University of Cambridge8, Stavanger University Hospital9, Oslo University Hospital10, Hospital Clínico San Carlos11, Mayo Clinic12, University of Western Brittany13, Rabin Medical Center14, Slovak Medical University15, Saarland University16, University of Barcelona17, University of Brescia18, University of Bern19, University of Erlangen-Nuremberg20, Leiden University Medical Center21
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
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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
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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
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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
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TL;DR: Authors/Task Force Members: Steen Dalby Kristensen*, Juhani Knuuti* (Chairperson) (Finland), Antti Saraste (Fin Finland), Stefan Anker (Germany), Hans Erik Bøtker (Denmark), Stefan De Hert (Belgium).
562 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
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9,185 citations
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5,737 citations
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4,790 citations
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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