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- Delewi, Ronak, et al.
(författare)
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Clinical and Procedural Characteristics Associated With Higher Radiation Exposure During Percutaneous Coronary Interventions and Coronary Angiography.
- 2013
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Ingår i: Circulation. Cardiovascular interventions. - 1941-7632. ; 6, s. 501-506
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: WE AIM TO STUDY THE CLINICAL AND PROCEDURAL CHARACTERISTICS ASSOCIATED WITH HIGHER RADIATION EXPOSURE IN PATIENTS UNDERGOING PERCUTANEOUS CORONARY INTERVENTIONS (PCIS) AND CORONARY ANGIOGRAPHY.METHODS AND RESULTS: OUR PRESENT STUDY INCLUDED ALL CORONARY ANGIOGRAPHY AND PCI PROCEDURES IN 5 PCI CENTERS IN THE WESTERN PART OF SWEDEN, BETWEEN JANUARY 1, 2008, AND JANUARY 19, 2012. THE RADIATION EXPOSURE AND CLINICAL DATA WERE COLLECTED PROSPECTIVELY IN THESE 5 PCI CENTERS IN SWEDEN AS PART OF THE SWEDISH CORONARY ANGIOGRAPHY AND ANGIOPLASTY REGISTRY (SCAAR). A PREDICTION MODEL WAS MADE FOR THE RADIATION EXPOSURE (DOSEAREA PRODUCT) EXPRESSED IN GYCM(2). A TOTAL OF 20 669 PROCEDURES WERE INCLUDED IN THE PRESENT STUDY, CONSISTING OF 9850 PCI AND 10 819 CORONARY ANGIOGRAPHY PROCEDURES. IN MULTIVARIABLE ANALYSES, BODY MASS INDEX (=1.04; CONFIDENCE INTERVAL [CI], 1.041.04; P0.001); HISTORY OF CORONARY ARTERY BYPASS GRAFT SURGERY (=1.32; CI, 1.281.32; P0.001); 2, 3, OR 4 TREATED LESIONS (2 TREATED LESIONS: =1.95; CI, 1.842.03; P0.001; 3 TREATED LESIONS: =2.34; CI, 2.162.53; P0.001; AND 4 TREATED LESIONS: =2.83; CI, 2.533.16; P0.001); AND CHRONIC TOTAL OCCLUSION LESIONS (=1.39; CI, 1.311.48; P0.001) WERE ASSOCIATED WITH THE HIGHEST RADIATION EXPOSURE. AFTER ADJUSTING FOR PROCEDURAL COMPLEXITY, RADIAL ACCESS ROUTE WAS NOT ASSOCIATED WITH INCREASED RADIATION EXPOSURE (=1.00; CI, 0.981.03; P=0.67).CONCLUSIONS: In the largest study population to assess radiation exposure, we found that high body mass index, history of coronary artery bypass graft surgery, number of treated lesions, and chronic total occlusions were associated with the highest patient radiation exposure. Radial access site was not associated with higher radiation exposure when compared with femoral approach.
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3. |
- Angerås, Oskar, 1976, et al.
(författare)
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Evidence for obesity paradox in patients with acute coronary syndromes : a report from the Swedish Coronary Angiography and Angioplasty Registry
- 2013
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Ingår i: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 34:5, s. 345-353
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Tidskriftsartikel (refereegranskat)abstract
- The obesity paradox refers to the epidemiological evidence that obesity compared with normal weight is associated with counter-intuitive improved health in a variety of disease conditions. The aim of this study was to investigate the relationship between body mass index (BMI) and mortality in patients with acute coronary syndromes (ACSs). We extracted data from the Swedish Coronary Angiography and Angioplasty Registry and identified 64 436 patients who underwent coronary angiography due to ACSs. In 54 419 (84.4) patients, a significant coronary stenosis was identified, whereas 10 017 (15.6) patients had no significant stenosis. Patients were divided into nine different BMI categories. The patients with significant stenosis were further subdivided according to treatment received such as medical therapy, percutaneous coronary intervention (PCI), or coronary artery by-pass grafting. Mortality for the different subgroups during a maximum of 3 years was compared using Cox proportional hazards regression with the lean BMI category (21.0 to 23.5 kg/m(2)) as the reference group. Regardless of angiographic findings [significant or no significant coronary artery disease (CAD)] and treatment decision, the underweight group (BMI 18.5 kg/m(2)) had the greatest risk for mortality. Medical therapy and PCI-treated patients with modest overweight (BMI category 26.528 kg/m(2)) had the lowest risk of mortality [hazard ratio (HR) 0.52; 95 CI 0.340.80 and HR 0.64; 95 CI 0.500.81, respectively]. When studying BMI as a continuous variable in patients with significant CAD, the adjusted risk for mortality decreased with increasing BMI up to approximate to 35 kg/m(2) and then increased. In patients with significant CAD undergoing coronary artery by-pass grafting and in patients with no significant CAD, there was no difference in mortality risk in the overweight groups compared with the normal weight group. In this large and unselected group of patients with ACSs, the relation between BMI and mortality was U-shaped, with the nadir among overweight or obese patients and underweight and normal-weight patients having the highest risk. These data strengthen the concept of the obesity paradox substantially.
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4. |
- Gizurarson, Sigfus, et al.
(författare)
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Electrophysiological Effects of Lysophosphatidylcholine on HL-1 Cardiomyocytes Assessed with a Microelectrode Array System
- 2012
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Ingår i: Cellular Physiology and Biochemistry. - : S. Karger AG. - 1015-8987 .- 1421-9778. ; 30:2, s. 477-488
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Tidskriftsartikel (refereegranskat)abstract
- Background: Sudden death due to malignant ventricular arrhythmias is the most important cause of death in acute myocardial infarction. Improved knowledge about the pathophysiology underlying these arrhythmias is essential in the search for new anti-arrhythmic strategies. Lysophosphatidylcholine (LPC), a hydrolysis product of (membrane) phospholipid degradation, is one of the most potent pro-arrhythmic substances that accumulate in the human heart during myocardial ischemia. The aim of this study was to set up and validate an in vitro experimental system for studies on the effects of LPC on electrophysiological parameters in beating cardiomyocytes. Methods and Results: Spontaneously beating HL-1 cardiomyocytes were cultured on multielectrode array microchips for three days for the recording of electrical activities in the form of field potentials (FP). FPs were recorded at baseline and after addition of 2, 4, 8, 12, 16, 20, and 24 mu M of LPC to the cell medium (n=9). We found that LPC could induce rapid effects on electrical parameters in the HL-1 cells. The overall half-maximal effective concentration (EC50) of LPC was around 12 mu M. The beating rate and peak-peak amplitude of FP thus decreased at concentrations >= 12 mu M and were inversely proportional to increased LPC concentration. The duration of FP was significantly prolonged with LPC above 12 mu M and was concentration-dependent. LPC delayed signal propagation, an effect which was mimicked by blocking gap junctions with heptanol and attenuated by pre-treatment with isoprenaline and atropine. Finally, asynchronous activity was induced by LPC at >12 mu M. Conclusions: LPC induced prompt and pronounced electrophysiological alterations that may underlie its observed pro-arrhythmic properties. Our in vitro model with HL-1 cells and microelectrode array system may be a useful tool for preclinical studies of electrophysiological effects of various pathophysiological concepts. Copyright (C) 2012 S Karger AG, Basel
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5. |
- Omerovic, Elmir, 1968, et al.
(författare)
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Levosimendan neither improves nor worsens mortality in patients with cardiogenic shock due to ST-elevation myocardial infarction.
- 2010
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Ingår i: Vascular health and risk management. - 1178-2048. ; 7:6, s. 657-663
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of this study was to evaluate the effect of levosimendan on mortality in cardiogenic shock (CS) after ST elevation myocardial infarction (STEMI). METHODS AND RESULTS: Data were obtained prospectively from the SCAAR (Swedish Coronary Angiography and Angioplasty Register) and the RIKS-HIA (Register of Information and Knowledge about Swedish Heart Intensive Care Admissions) about 94 consecutive patients with CS due to STEMI. Patients were classified into levosimendan-mandatory and levosimendan-contraindicated cohorts. Inotropic support with levosimendan was mandatory in all patients between January 2004 and December 2005 (n = 46). After the SURVIVE and REVIVE II studies were presented, levosimendan was considered contraindicated and was not used in consecutive patients between December 2005 and December 2006 (n = 48). The cohorts were similar with respect to pre-treatment characteristics and concomitant medications. There was no difference in the incidence of new-onset atrial fibrillation, in-hospital cardiac arrest and length of stay at the coronary care unit. There was no difference in adjusted mortality at 30 days and at one year. CONCLUSION: The use of levosimendan neither improves nor worsens mortality in patients with CS due to STEMI. Well-designed randomized clinical trials are needed to define the role of inotropic therapy in the treatment of CS.
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- Redfors, Björn, et al.
(författare)
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Effects of doxorubicin on myocardial expression of apolipoprotein-B.
- 2012
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Ingår i: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1651-2006 .- 1401-7431. ; 46:2
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Doxorubicin (DOX) is an effective antitumor agent against a variety of human malignancies but is associated with deleterious side effects, including myocardial damage and heart failure. Myocardial apoB-containing lipoprotein (apoB) is upregulated post myocardial infarction and has been shown to be cardioprotective in this setting by unloading excessive lipid. The aim of this study was to investigate whether apoB expression is increased also in DOX-induced heart failure and whether apoB overexpression protects the heart in DOX-induced myocardial injury. Design: Cardiac function and energy metabolism was studied in mice and rats 24 hours after intraperitoneally administered DOX. Results: We found that the content of apoB was decreased in rat myocardium 24 hours after DOX injection. In contrast, apoB content was increased in the infarcted myocardium of rats 24 hours post ischemia-reperfusion. Moreover, transgenic mice overexpressing apoB had better cardiac function and lower intracellular lipid accumulation compared to wild type mice 24h post DOX. Conclusions: Our findings indicate that depression of the myocardial apoB system may contribute to DOX-induced cardiac injury and that overexpression of apoB is protective, not only in ischemically damaged myocardium, but also in DOX-induced heart failure.
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7. |
- Redfors, Björn, et al.
(författare)
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Effects of doxorubicin on myocardial expression of apolipoprotein-B.
- 2012
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Ingår i: Scandinavian Cardiovascular Journal. - : Informa UK Limited. - 1401-7431 .- 1651-2006. ; 46:2, s. 93-98
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Tidskriftsartikel (refereegranskat)abstract
- Abstract OBJECTIVE: Doxorubicin (DOX) is an effective antitumour agent against a variety of human malignancies but is associated with deleterious side effects, including myocardial damage and heart failure. Myocardial apoB-containing lipoprotein (apoB) is upregulated post myocardial infarction and has been shown to be cardioprotective in this setting by unloading excessive lipid. The aim of this study was to investigate whether apoB expression is increased also in DOX-induced heart failure and whether apoB overexpression protects the heart in DOX-induced myocardial injury. DESIGN: Cardiac function and energy metabolism was studied in mice and rats 24 hours after intraperitoneally administered DOX. RESULTS: We found that the content of apoB was decreased in rat myocardium 24 hours after DOX injection. In contrast, apoB content was increased in the infarcted myocardium of rats 24 hours post ischemia-reperfusion. Moreover, transgenic mice overexpressing apoB had better cardiac function and lower intracellular lipid accumulation compared to wild type mice 24 hours post DOX.
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8. |
- Redfors, Björn, et al.
(författare)
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Takotsubo triggered by acute myocardial infarction: a common but overlooked syndrome?
- 2014
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Ingår i: Journal of geriatric cardiology : JGC. - 1671-5411. ; 11:2, s. 171-3
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Tidskriftsartikel (refereegranskat)abstract
- Takotsubo cardiomyopathy (TCM) is an acute cardiac syndrome characterized by extensive, but potentially reversible, left ventricular dysfunction in the absence of an explanatory coronary obstruction. Thus, TCM is distinct from coronary artery disease (CAD) and acute myocardial infarction (AMI). However, substantial evidence for co-existing CAD in some TCM patients exist. Herein, we take this association one step further and present a case in which the patient simultaneously suffered from AMI and TCM, and in which we believe that a primary coronary event triggered TCM. An 88-year-old female presented with chest pain. Echocardiography revealed apical akinesia with hypercontractile bases. An occluded diagonal branch with suspected acute plaque rupture was identified on the angiogram, but could not explain the extent of akinesia. Cardiac function recovered completely. Thus, this patient adhered to current diagnostic criteria for TCM. TCM is a well-known complication for other conditions associated with somatic stress. It is therefore intuitive to assume that AMI, which also associates with somatic stress and elevated catecholamine, can cause TCM. Our case illustrates that TCM and AMI may occur simultaneously. Although causality cannot be conclusively inferred from this association, the somatic stress associated with AMI may have caused TCM in this patient.
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- Råmunddal, Truls, 1973, et al.
(författare)
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Overexpression of apolipoprotein B attenuates pathologic cardiac remodeling and hypertrophy in response to catecholamines and after myocardial infarction in mice.
- 2012
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Ingår i: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 0036-5513 .- 1502-7686. ; 72:3, s. 230-236
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Tidskriftsartikel (refereegranskat)abstract
- Abstract Introduction. The heart produces apolipoprotein (apo) B-containing lipoproteins which enables cardiac export of potentially cardiotoxic lipids. We hypothesized that overexpression of apoB attenuates the pathologic cardiac remodeling and hypertrophic response following pathological stimuli such as chronic adrenergic overstimulation and myocardial infarction (MI). Methods. Cardiac hypertrophy was induced by a chronic infusion of isoproterenol (ISO) 15 mg/kg/day for 3 weeks in human apoB transgenic mice (n9) and in non-transgenic wild-type mice (n10). As controls, apoB transgenic (N10) and wild-type mice (N10) saline infusions were used. Transthoracic echocardiography was performed at baseline and after 3 weeks of treatment to evaluate left ventricular (LV) function and morphology. To investigate the effects of expression on postinfarct hypertrophic response we induced MI in apoB transgenic mice (n8) and in wild-type controls (n11). The hearts were explanted and weighed 6 weeks post MI. Results. At baseline, WT mice had higher BW and LV mass (LVM) compared to the apoB mice. The increase in LV mass and dimensions after 3 weeks of treatment with ISO was significantly lower while systolic function was signifi cantly better in the apoB group. Six weeks post MI the apoB mice had significantly lower heart weight and heart weight to body weight ratio. The infarct size was similar in both groups. Conclusion. Overexpression of apoB attenuates the pathologic remodeling and hypertrophic response to chronic adrenergic stimulation and MI. Our results indicate that cardiac expression of apoB-containing lipoproteins might be an important regulator of myocardial structure and function.
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- Scharin Täng, Margareta, 1962, et al.
(författare)
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Importance of circulating IGF-1 for normal cardiac morphology, function and post infarction remodeling
- 2012
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Ingår i: Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society. - : Elsevier BV. - 1096-6374. ; 22:6, s. 206-211
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Tidskriftsartikel (refereegranskat)abstract
- IGF-1 plays an important role in cardiovascular homeostasis, and plasma levels of IGF-1 correlate inversely with systolic function in heart failure. It is not known to what extent circulating IGF-1 secreted by the liver and local autocrine/paracrine IGF-1 expressed in the myocardium contribute to these beneficial effects on cardiac function and morphology. In the present study, we used a mouse model of liver-specific inducible deletion of the IGF-1 gene (LI-IGF-1 -/- mouse) in an attempt to evaluate the importance of circulating IGF-I on cardiac morphology and function under normal and pathological conditions, with an emphasis on its regulatory role in myocardial phosphocreatine metabolism. Echocardiography was performed in LI-IGF-1 -/- and control mice at rest and during dobutamine stress, both at baseline and post myocardial infarction (MI). High-energy phosphate metabolites were compared between LI-IGF-1 -/- and control mice at 4weeks post MI. We found that LI-IGF-1 -/- mice had significantly greater left ventricular dimensions at baseline and showed a greater relative increase in cardiac dimensions, as well as deterioration of cardiac function, post MI. Myocardial creatine content was 17.9% lower in LI-IGF-1 -/- mice, whereas there was no detectable difference in high-energy nucleotides. These findings indicate an important role of circulating IGF-1 in preserving cardiac structure and function both in physiological settings and post MI.
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- Schultz, Tomas, 1972, et al.
(författare)
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Stress-Induced Cardiomyopathy in Sweden: Evidence for Different Ethnic Predisposition and Altered Cardio-Circulatory Status
- 2012
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Ingår i: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 122:3, s. 180-186
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Tidskriftsartikel (refereegranskat)abstract
- Background: In this paper, we report about new insights regarding clinical course, long-term outcome, ethnic/genetic predisposition and cardio-circulatory status in the large stress-induced cardiomyopathy (SIC) cohort from Sweden. Methods and Results: We have included 115 consecutive SIC patients between January 2005 and January 2010 at Sahlgrenska University Hospital in Gothenburg. Hemodynamic status and sympathetic nerve activity were evaluated and compared with those of healthy controls. Mean age was 64, and 14% were males. Thirty-day and 3-year mortality was 6 and 10%, respectively. Eleven percent had ischemic heart disease, 3% developed thromboembolic complications, 6% had cardiac arrest and 14% developed cardiogenic shock. The great majority of SIC patients (93%) were ethnic Swedes. In three families, several close relatives developed SIC. Fourteen percent developed two or more episodes of SIC. Hemodynamic evaluation has shown subnormal systemic vascular resistance, 22% lower sympathetic activity and preserved cardiac output in SIC patients. Conclusions: SIC affects both men and women of different ages and is associated with significant short- and long-term mortality. There is a strong signal for the presence of ethnic/genetic predisposition to develop SIC. Sympathetic activity and systemic vascular resistance are lower in SIC patients, suggesting that SIC is a cardio-circulatory phenomenon. Copyright (C) 2012 S. Karger AG, Basel
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