Cardiac Sympathetic Denervation in Patients With Coronary Artery Disease Without Previous Myocardial Infarction

1997 ◽  
Vol 80 (3) ◽  
pp. 273-277 ◽  
Author(s):  
Juha Hartikainen ◽  
Juha Mustonen ◽  
Jyrki Kuikka ◽  
Esko Vanninen ◽  
Raimo Kettunen
2005 ◽  
Vol 58 (2) ◽  
pp. 218-221 ◽  
Author(s):  
Alejandro I. Pérez Cabeza ◽  
Juan J. Gómez Doblas ◽  
Luis Morcillo Hidalgo ◽  
Fernando Cabrera Bueno ◽  
Manuel F. Jiménez Navarro ◽  
...  

Author(s):  
A Nichols ◽  
J Owen ◽  
K L Kaplan ◽  
P J Cannon ◽  
H L Nossel ◽  
...  

To determine whether activation of platelets and coagulation is present in patients with coronary artery disease, plasma levels of platelet factor 4 (PF4), β-thromboglobulin (βTG), and fibrinopeptide A (FPA) were measured by radioimmunoassay in patients subjected to coronary angiography. The patients were divided into those with normal coronary angiograms (Group I, n = 14), those with coronary artery disease (> 70% narrowing) but no previous myocardial infarction (Group II, n = 32), and those with coronary artery disease and documented previous myocardial infarction (Group III, n = 36). The three groups did not differ in sex, incidence of hypertension or diabetes, serum cholesterol, HDL cholesterol, BUN or platelet count. Geometric mean values for the three groups were FPA: 0.77, 0.81 and 1.01 pmol/ml respectively, βTG: 22.7, 21.6 and 33.2 ng/ml respectively, and PF4: 5.7, 5.8 and 8.3 ng/ml respectively. When the data were tested by analysis of variance, significant elevations of βTG (p< .01) and PF4 (p< .05) were found in Group III but there were no other significant changes. When Group III was subdivided into patients with and without ventricular aneurysm, BTG and FPA levels were found to be higher in patients with aneurysm than without: βTG 45.9 vs. 30.3 ng/ml and FPA 1.64 vs. 0.88 pmol/ml (p< .05 for each). βTG levels were also higher in patients with congestive heart failure (p< .01) and showed an inverse correlation with left ventricular ejection fraction (p< .05) and a direct correlation with the extent of left ventricular asynergy (p< .01). In conclusion, elevations in βTG and PF4 were associated with previous infarction, not with coronary artery disease. These changes are thought to reflect platelet reaction with the damaged ventricular wall. Elevations in FPA were seen only in patients with ventricular aneurysm and may reflect mural thrombus within the aneurysm.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Konstantinos Mourouzis ◽  
Gerasimos Siasos ◽  
Evangelos Oikonomou ◽  
Marina Zaromitidou ◽  
Vicky Tsigkou ◽  
...  

Abstract Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), can exert proinflammatory as well as proatherogenic properties on the vascular wall. The current study sought to evaluate the influence of high Lp-PLA2 levels on indices of arterial wall properties in patients with stable coronary artery disease (CAD). Methods Three hundred seventy-four consecutive patients with stable CAD (mean age 61 ± 11 years, 89% males) were enrolled in this single-center cross-sectional study. Flow-mediated dilation (FMD) was used to assess endothelial function and augmentation index (AIx) of the central aortic pressure was used to assess reflected waves. ELISA was used to determine Lp-PLA2 serum levels. Results After dividing the participants in 3 equal groups based on the tertiles of circulating Lp-PLA2 values, no significant differences were demonstrated between those in the 3rd tertile with Lp-PLA2 values > 138 μg/L, in the 2nd tertile with Lp-PLA2 values between 101 and 138 μg/L and in the 1st tertile (Lp-PLA2 values < 101 μg/L) regarding age, male gender, smoking habits, family history of CAD or history of a previous myocardial infarction, diabetes mellitus, arterial hypertension, hyperlipidemia, duration of CAD and treatment with relevant medication. Importantly, subjects with Lp-PLA2 values in the highest tertile, had significantly reduced FMD values compared to the middle and lower tertile (4.43 ± 2.37% vs. 4.61 ± 1.97% vs. 5.20 ± 2.52% respectively, P = 0.03). Patients in the highest tertile of Lp-PLA2 values had significantly higher AIx values (24.65 ± 8.69% vs. 23.33 ± 9.65%, P = 0.03), in comparison to the lowest tertile, with Lp-PLA2 values < 101 μg/L. A linear regression analysis showed that Lp-PLA2 values > 138 μg/L negatively correlated to FMD [b = − 0.45 (95% CI: − 0.79 – -0.11), P = 0.01] and AIx values [b = 1.81 (95% CI: 0.57–3.05), P < 0.001] independently of cofounders like gender, age, diabetes mellitus, arterial hypertension, dyslipidemia, smoking habits, family history of CAD, history of previous myocardial infarction, serum glucose, circulating lipid levels, duration of CAD, antihypertensive medication, antidiabetic drugs, statin therapy and treatment with β-blockers. Conclusions Elevated Lp-PLA2 levels relate to endothelial dysfunction and arterial stiffness in patients with stable CAD independently from classical risk factors for CAD, statin use, antihypertensive treatment, and duration of the disease.


1988 ◽  
Vol 60 (03) ◽  
pp. 372-376 ◽  
Author(s):  
Kurt Huber ◽  
Danuta Rosc ◽  
Irene Resch ◽  
Ernst Schuster ◽  
Dietmar H Glogar ◽  
...  

SummaryA decrease in the fibrinolytic potential, mainly due to an elevation of plasminogen activator inhibitor (PAI), has been described in patients with stable coronary artery disease and a previous myocardial infarction. We investigated plasma levels of PAI and tissue plasminogen activator (t-PA) and their possible circadian variations in patients with unstable coronary artery disease (CAD). Sixty-three patients were studied for at least 2 consecutive days during their stay at the coronary care unit (CCU). Diurnal plasma fluctuations in PAI and t-PA and onset of further myocardial ischemic episodes were monitored. As controls we used 22 age-matched patients submitted to the clinic because of non cardiac chest pain or valvular disease who revealed no evidence of CAD. PAI levels were significantly elevated in patients with unstable CAD (p < 0.0001) but were not influenced by the extent of underlying CAD, history of previous myocardial infarction, known risk factors for CAD, or by extent of myocardial damage. The circadian variation of PAI levels with peak values between midnight and 6 A. M. found in controls was still present in patients but at a higher level. Preservation of circadian pattern in PAI plasma levels despite myocardial ischemic attacks indicates that elevation of PAI is rather not caused by a reactive phenomenon. On the other hand, elevated PAI levels and episodes of severe myocardial ischemia exhibiting a median time of onset at 10 A. M. seem to be closely related.


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