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[Adaptation of the myocardium to decreased coronary flow]

https://arctichealth.org/en/permalink/ahliterature54934
Source
Duodecim. 1994;110(8):777-9
Publication Type
Article
Date
1994
Author
K. Ylitalo
K. Peuhkurinen
Author Affiliation
Sisätautien klinikka, Oulu.
Source
Duodecim. 1994;110(8):777-9
Date
1994
Language
Finnish
Publication Type
Article
Keywords
Humans
Myocardial Ischemia - diagnosis - physiopathology
Myocardial Stunning
Myocardium - metabolism - pathology
Necrosis
PubMed ID
8586035 View in PubMed
Less detail

Adaptation to myocardial ischemia during repeated dynamic exercise in relation to findings at cardiac catheterization.

https://arctichealth.org/en/permalink/ahliterature46459
Source
Am Heart J. 1996 Apr;131(4):689-97
Publication Type
Article
Date
Apr-1996
Author
K. Ylitalo
L. Jama
P. Raatikainen
K. Peuhkurinen
Author Affiliation
Department of Internal Medicine, Division of Cardiology, Oulu University Central Hospital, Finland.
Source
Am Heart J. 1996 Apr;131(4):689-97
Date
Apr-1996
Language
English
Publication Type
Article
Keywords
Angina Pectoris - etiology - physiopathology
Collateral Circulation
Coronary Circulation
Electrocardiography
Exercise Test
Female
Heart Catheterization
Humans
Male
Middle Aged
Myocardial Ischemia - complications - physiopathology
Oxygen consumption
Severity of Illness Index
Survival Analysis
Abstract
It has been suggested that the myocardium is able to recruit endogenous protective mechanisms in response to repeated ischemia and reperfusion. We set out to study whether this is manifested in patients with coronary artery disease in the form of fewer signs of myocardial ischemia during the second of two successive exercise tests and whether any relations exist between ischemia adaptation and findings at cardiac catheterization. Twenty-one patients with typical angina pectoris symptoms underwent two repeated bicycle exercise tests with identical protocols, followed by cardiac catheterization and coronary angiography the next day. The first exercise test was discontinued whenever a 2 mm ST depression in the electrocardiogram (ECG) was achieved or further exercise was limited by symptoms. The second exercise test was performed after disappearance of the symptoms or ST depression or both. Kaplan-Meier survival analysis for the appearance of a 1 mm ST depression demonstrated improved ischemia tolerance during the second test, when the required time for its appearance was significantly longer (6.5 +/- 0.8 min vs 4.5 +/- 0.5 min; p = 0.005). The maximal intensity of anginal pain was lower during the second exercise (2.2 +/- 1.0 min vs 0.7 +/- 0.3 min in Borg's scale; p
PubMed ID
8721640 View in PubMed
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Adaptation to myocardial ischemia during repeated ventricular pacing in patients with coronary artery disease.

https://arctichealth.org/en/permalink/ahliterature46178
Source
Scand Cardiovasc J. 2000;34(2):134-41
Publication Type
Article
Date
2000
Author
K. Ylitalo
K. Peuhkurinen
Author Affiliation
Department of Internal Medicine, University of Oulu, Finland.
Source
Scand Cardiovasc J. 2000;34(2):134-41
Date
2000
Language
English
Publication Type
Article
Keywords
Cardiac Pacing, Artificial
Coronary Disease - therapy
Female
Hemodynamic Processes
Humans
Male
Middle Aged
Myocardial Ischemia - prevention & control
Abstract
OBJECTIVE: The purpose of our study was to evaluate whether repeated ventricular pacing is able to induce adaptation against ischemia in coronary artery disease patients. DESIGN: Fifteen patients with documented coronary artery disease were subjected to two successive periods of rapid ventricular pacing (150 bpm) of equal length (295+/-33 s), the first being limited by intolerable anginal pain. The second pacing period, of the same length as the first, was initiated after the disappearance of angina and ST depression, the mean resting time being 433+/-30 s. Blood samples for the determination of transcardiac differences in glucose, lactate, free fatty acids, K+, pCO2, pH, oxygen saturation and noradrenaline were taken from the femoral artery and coronary sinus before and at the end of each pacing period. The mechanical performance of the hearts was followed by continuous monitoring of intra-arterial blood pressure and pulmonary capillary wedge pressure, and the observed adaptation in the measured variables during the successive pacing tests was correlated with the duration of angina, severity of coronary artery disease and degree of collateralization. RESULTS: Changes in the transcardiac pH and K+ differences, ST segment and pulmonary capillary wedge pressure were less pronounced during the second pacing period. The subgroup with net lactate production before or after the first pacing period demonstrated metabolic adaptation manifested as improved lactate extraction during the second pacing period. Rate-pressure product and oxygen extraction, and thus presumably also overall oxygen consumption and oxygen delivery, were similar during both tests. The magnitude of adaptation did not correlate with the duration of angina, severity of coronary artery disease or overall collateral score. CONCLUSION: Rapid ventricular pacing is able to induce adaptation to myocardial ischemia, but the exact mechanisms in this process remain to be elucidated.
PubMed ID
10872698 View in PubMed
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[Endogenous defense mechanisms of myocardium]

https://arctichealth.org/en/permalink/ahliterature54565
Source
Duodecim. 1997;113(22):2277-82
Publication Type
Article
Date
1997
Author
K. Ylitalo
K. Peuhkurinen
Author Affiliation
OYS:n sisätautien klinikka, Oulu.
Source
Duodecim. 1997;113(22):2277-82
Date
1997
Language
Finnish
Publication Type
Article
Keywords
Adaptation, Physiological
Humans
Ischemic Preconditioning, Myocardial
Myocardial Infarction - metabolism
Myocardium - metabolism
PubMed ID
10892131 View in PubMed
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Genomewide scan for familial combined hyperlipidemia genes in finnish families, suggesting multiple susceptibility loci influencing triglyceride, cholesterol, and apolipoprotein B levels.

https://arctichealth.org/en/permalink/ahliterature202403
Source
Am J Hum Genet. 1999 May;64(5):1453-63
Publication Type
Article
Date
May-1999
Author
P. Pajukanta
J D Terwilliger
M. Perola
T. Hiekkalinna
I. Nuotio
P. Ellonen
M. Parkkonen
J. Hartiala
K. Ylitalo
J. Pihlajamäki
K. Porkka
M. Laakso
J. Viikari
C. Ehnholm
M R Taskinen
L. Peltonen
Author Affiliation
Department of Human Molecular Genetics, National Public Health Institute and Department of Medical Genetics, University of Helsinki, Germany.
Source
Am J Hum Genet. 1999 May;64(5):1453-63
Date
May-1999
Language
English
Publication Type
Article
Keywords
Adult
Aged
Apolipoproteins B - blood
Cholesterol - blood
Chromosome Mapping
Female
Finland - ethnology
Genetic Predisposition to Disease
Genome, Human
Humans
Hyperlipidemia, Familial Combined - classification - genetics
Lod Score
Male
Middle Aged
Triglycerides - blood
Abstract
Familial combined hyperlipidemia (FCHL) is a common dyslipidemia predisposing to premature coronary heart disease (CHD). The disease is characterized by increased levels of serum total cholesterol (TC), triglycerides (TGs), or both. We recently localized the first locus for FCHL, on chromosome 1q21-q23. In the present study, a genomewide screen for additional FCHL loci was performed. In stage 1, we genotyped 368 polymorphic markers in 35 carefully characterized Finnish FCHL families. We identified six chromosomal regions with markers showing LOD score (Z) values >1.0, by using a dominant mode of inheritance for the FCHL trait. In addition, two more regions emerged showing Z>2.0 with a TG trait. In stage 2, we genotyped 26 more markers and seven additional FCHL families for these interesting regions. Two chromosomal regions revealed Z>2.0 in the linkage analysis: 10p11.2, Z=3.20 (theta=.00), with the TG trait; and 21q21, Z=2.24 (theta=.10), with the apoB trait. Furthermore, two more chromosomal regions produced Z>2.0 in the affected-sib-pair analysis: 10q11.2-10qter produced Z=2.59 with the TC trait and Z=2.29 with FCHL, and 2q31 produced Z=2.25 with the TG trait. Our results suggest additional putative loci influencing FCHL in Finnish families, some potentially affecting TG levels and some potentially affecting TC or apoB levels.
Notes
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PubMed ID
10205279 View in PubMed
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Mechanisms of ischemic preconditioning in rat myocardium. Roles of adenosine, cellular energy state, and mitochondrial F1F0-ATPase.

https://arctichealth.org/en/permalink/ahliterature54766
Source
Circulation. 1995 Jun 1;91(11):2810-8
Publication Type
Article
Date
Jun-1-1995
Author
K. Vuorinen
K. Ylitalo
K. Peuhkurinen
P. Raatikainen
A. Ala-Rämi
I E Hassinen
Author Affiliation
Department of Medical Biochemistry, University of Oulu, Finland.
Source
Circulation. 1995 Jun 1;91(11):2810-8
Date
Jun-1-1995
Language
English
Publication Type
Article
Keywords
Adenosine - physiology
Adenosine Triphosphate - metabolism
Animals
Energy Metabolism - physiology
Magnetic Resonance Spectroscopy - diagnostic use
Male
Mitochondria, Heart - enzymology
Myocardial Ischemia - physiopathology
Myocardial Reperfusion Injury - physiopathology - prevention & control
Myocardium - metabolism
Perfusion
Proton-Translocating ATPases - metabolism - physiology
Rats
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Time Factors
Abstract
BACKGROUND: Adenosine has been proposed as one mediator for the preconditioning effect in the myocardium of some animals, but recent investigations have shown that this may not be the mechanism in the rat heart, although the effect itself is clearly demonstrable. The cellular energy state has been shown to be better in preconditioned hearts, and the role of ATP consumption has been discussed. The role of inhibition of mitochondrial F1F0-ATPase as a mechanism for the preservation of ATP in preconditioned hearts remains controversial. METHODS AND RESULTS: Three-minute global ischemia followed by 9 minutes of reperfusion was used to precondition Langendorff-perfused rat hearts, and control hearts were perfused under normoxic conditions for the same time. The duration of sustained ischemia in both groups of hearts was 21 minutes, after which the hearts were reperfused for 15 minutes to evaluate their mechanical and metabolic recovery. Separate experiments were performed for tissue metabolite determinations, mitochondrial ATPase activity measurements, and 31P nuclear magnetic resonance studies. The recovery of the rate-pressure product was better in the preconditioned group. Three-minute preconditioning ischemia caused inhibition of the mitochondrial ATPase that persisted throughout the 9-minute intervening reperfusion so that at the early stages of sustained ischemia the enzyme activity was still more inhibited in preconditioned hearts. ATP was better preserved in preconditioned hearts than in control hearts during sustained ischemia. The accumulation of adenosine and its degradation products during sustained ischemia was greater in the control group. More lactate and H+ ions accumulated in this group, indicating higher anaerobic glycolysis. Also, inhibition of mitochondrial ATPase by oligomycin slowed ATP depletion during ischemia. CONCLUSIONS: The results indicate that preconditioning causes inhibition of rat heart mitochondrial ATPase that persists during reperfusion so that the enzyme is inhibited from the very beginning of the sustained ischemia. This inhibition leads to sparing of high-energy phosphates and improves the time-averaged energy state during ischemia. Although a causal relationship is difficult to prove, this reversible inhibition may contribute to postischemic recovery of the heart.
Notes
Comment In: Circulation. 1996 Jan 1;93(1):200-28616933
PubMed ID
7758188 View in PubMed
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Natriuretic peptides and mortality after stroke.

https://arctichealth.org/en/permalink/ahliterature47075
Source
Stroke. 2005 May;36(5):1016-20
Publication Type
Article
Date
May-2005
Author
A M Mäkikallio
T H Mäkikallio
J T Korpelainen
O. Vuolteenaho
J M Tapanainen
K. Ylitalo
K A Sotaniemi
H V Huikuri
V V Myllylä
Author Affiliation
Graduate School of Circumpolar Wellbeing, Health, and Adaptation, Centre for Arctic Medicine, University of Oulu, Finland. anne.makikallio@mail.suomi.net
Source
Stroke. 2005 May;36(5):1016-20
Date
May-2005
Language
English
Publication Type
Article
Keywords
Aged
Atrial Natriuretic Factor - blood
Brain Infarction - blood
Case-Control Studies
Cerebrovascular Accident - blood - diagnosis - mortality
Comparative Study
Female
Humans
Male
Natriuretic Peptide, Brain
Nerve Tissue Proteins - blood
Peptide Fragments - blood
Prognosis
Prospective Studies
Protein Precursors - blood
Research Support, Non-U.S. Gov't
Risk factors
Abstract
BACKGROUND AND PURPOSE: Measurement of natriuretic peptides provides prognostic information in various patient populations. The prognostic value of natriuretic peptides among patients with acute stroke is not known, although elevated peptide levels have been observed. METHODS: A series of 51 patients (mean age, 68+/-11 years) with first-ever ischemic stroke underwent a comprehensive clinical examination and measurements of plasma atrial natriuretic peptides (N-ANP) and brain natriuretic peptides (N-BNP) in the acute phase of stroke. The patients were followed-up for 44+/-21 months. Risk factors for all-cause mortality were assessed. Control populations, matched for gender and age, consisted of 51 patients with acute myocardial infarction (AMI) and 25 healthy subjects. RESULTS: Plasma concentrations of N-ANP (mean+/-SD, 988+/-993 pmol/L) and N-BNP (751+/-1608 pmol/L) in the stroke patients were at the same level as those in the AMI patients (NS for both), but significantly higher than those of the healthy subjects (358+/-103 pmol/L, P
PubMed ID
15802631 View in PubMed
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No evidence for ischemic preconditioning during repeated vessel occlusion in coronary angioplasty.

https://arctichealth.org/en/permalink/ahliterature54628
Source
Int J Cardiol. 1996 Aug;55(3):227-37
Publication Type
Article
Date
Aug-1996
Author
K. Ylitalo
J. Airaksinen
M. Ikäheimo
H. Ruskoaho
K. Peuhkurinen
Author Affiliation
Department of Internal Medicine, University of Oulu, Finland.
Source
Int J Cardiol. 1996 Aug;55(3):227-37
Date
Aug-1996
Language
English
Publication Type
Article
Keywords
Angioplasty, Transluminal, Percutaneous Coronary
Atrial Natriuretic Factor - blood
Catecholamines - blood
Constriction, Pathologic
Coronary Disease - therapy
Female
Humans
Ischemic Preconditioning, Myocardial
Male
Middle Aged
Myocardium - metabolism
Pulmonary Wedge Pressure
Research Support, Non-U.S. Gov't
Abstract
Coronary angioplasty has been the favoured model in studying ischemic preconditioning in humans, but results have remained controversial, possibly due to some artefacts related to coronary balloon angioplasty as an ischemia model. We examined this issue by monitoring the sequential metabolic, functional and neurohumoral changes during repeated vessel occlusion in coronary angioplasty performed in patients with chronic angina pectoris. Two groups of patients undergoing two successive balloon inflations of approximately 2 min duration were studied. These balloon inflations were preceded by a short inflation performed immediately after introduction of the balloon into the stenosis. The aim of this primary inflation was to establish adequate coronary blood flow with the deflated balloon in the stenosis and to guarantee that the subsequent two balloon inflations were truly comparable in time. Group I consisted of 23 patients, in whom the changes in the degree of angina, pulmonary capillary wedge pressure (PCWP), atrial natriuretic peptide (ANP) and circulating catecholamines during the procedure were studied. The sequential changes in myocardial metabolism were monitored in group II of nine patients by determining the lactate extraction ratios and femoroarterial coronary sinus (Fa-CS) differences in pH and pCO2 before and after each balloon inflation. In group I, PCWP and total catecholamines increased similarly during both balloon inflations, but ANP remained unchanged. In group II patients the lactate extraction ratios turned negative, the Fa-CS pH-differences increased and the pCO2-differences decreased during vessel occlusions, the changes being somewhat more prominent during the second balloon inflation. To study adaptation to ischemia, the group I patients were divided into two subgroups with and without signs of ischemic dysfunction during balloon inflations (PCWP increase > 5 mmHg and
PubMed ID
8877422 View in PubMed
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Phenotype expression in familial combined hyperlipidemia.

https://arctichealth.org/en/permalink/ahliterature207605
Source
Atherosclerosis. 1997 Sep;133(2):245-53
Publication Type
Article
Date
Sep-1997
Author
K V Porkka
I. Nuotio
P. Pajukanta
C. Ehnholm
L. Suurinkeroinen
M. Syvänne
T. Lehtimäki
A T Lahdenkari
S. Lahdenperä
K. Ylitalo
M. Antikainen
M. Perola
O T Raitakari
P. Kovanen
J S Viikari
L. Peltonen
M R Taskinen
Author Affiliation
Department of Medicine, HUCH, University of Helsinki, Finland. kimmo.porkka@muikku.huch.fi
Source
Atherosclerosis. 1997 Sep;133(2):245-53
Date
Sep-1997
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Anthropometry - methods
Apolipoproteins B - blood
Child
Child, Preschool
Cholesterol - blood
Female
Finland - epidemiology
Gene Expression
Humans
Hyperlipidemia, Familial Combined - diagnosis - epidemiology - genetics
Life Style
Lipids - blood - genetics
Male
Middle Aged
Phenotype
Triglycerides - blood
Abstract
Familial combined hyperlipidaemia (FCHL) is one of the most common hereditary disorders predisposing to early coronary death. The affected family members have elevations of serum total cholesterol, triglycerides or both. Despite intensive research efforts the genetic and metabolic defects underlying this complex disorder are still unknown. To dissect the metabolism and genetics of FCHL the phenotype of an individual must be precisely defined. We assessed the influence of different diagnostic criteria on the phenotype definition and studied factors affecting the phenotype expression in 16 large Finnish families (n = 255) with FCHL. The fractile cut-points used to define abnormal lipid values had a profound influence on the diagnosis of FCHL. If the 90th percentile cut-point was used, approximately 45% of the family members were affected, in concord with the presumed dominant mode of transmission for FCHL. If the 95th percentile was used only 22% of study subjects were affected. To characterize the metabolic differences or similarities between the different lipid phenotypes, we determined very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) particles separated by ultracentrifugation. In linkage analysis no single ultracentrifugation variable could discriminate reliably affected family members from non-affected family members. Our data emphasizes the need for re-evaluation of FCHL diagnostic criteria. Preferably, the diagnosis should be based on a single, reliable metabolic marker.
PubMed ID
9298685 View in PubMed
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Reduced hormone-sensitive lipase activity is not a major metabolic defect in Finnish FCHL families.

https://arctichealth.org/en/permalink/ahliterature196048
Source
Atherosclerosis. 2000 Dec;153(2):373-81
Publication Type
Article
Date
Dec-2000
Author
K. Ylitalo
V. Large
P. Pajukanta
S. Reynisdottir
K V Porkka
J. Vakkilainen
I. Nuotio
M R Taskinen
P. Arner
Author Affiliation
Department of Medicine, University of Helsinki, Finland.
Source
Atherosclerosis. 2000 Dec;153(2):373-81
Date
Dec-2000
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Adult
Aged
Down-Regulation
Female
Finland - epidemiology
Humans
Hyperlipidemia, Familial Combined - epidemiology - metabolism
Male
Middle Aged
Pedigree
Sterol Esterase - metabolism
Abstract
The pathogenetic mechanisms behind familial combined hyperlipidemia (FCHL) are unknown. However, exaggerated postprandial lipemia and excessive serum free fatty acid (FFA) concentrations have drawn attention to altered lipid storage and lipolysis in peripheral adipose tissue. Hormone-sensitive lipase (HSL) is the enzyme responsible for intracellular lipolysis in adipocytes and a decrease of adipocyte HSL activity has been demonstrated in Swedish FCHL subjects. The aim of the study was to investigate if adipose tissue HSL activity had any effect on lipid phenotype and if low HSL activity and FCHL were linked in Finnish FCHL families. A total of 48 family members from 13 well-characterized Finnish FCHL families and 12 unrelated spouses participated in the study. FCHL patients with different lipid phenotypes (IIA, IIB, IV) did not differ in adipose tissue HSL activity from each other or from the 12 normolipidemic spouses (P = 0.752). In parametric linkage analysis using an affecteds-only strategy the low adipose tissue HSL activity was not significantly linked with FCHL phenotype. However, we found a significant sibling-sibling correlation for the HSL trait (0.51, P
PubMed ID
11164426 View in PubMed
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14 records – page 1 of 2.