Effectiveness of Long-term Heparin-induced Extracorporeal LDL Precipitation (HELP) in Improving Coronary Calcifications

2003 ◽  
Vol 26 (3) ◽  
pp. 252-255 ◽  
Author(s):  
A. Ramunni ◽  
L.F. Morrone ◽  
G. Baldassarre ◽  
E. Montagna ◽  
A. Saracino ◽  
...  

There is clear clinical evidence that a drastic lowering of plasma LDL- Cholesterol (LDL) concentrations significantly reduces the rate of total and coronary mortality as well as the incidence of cardiovascular events in high risk hypercholesterolemic patients. We describe the case of a 51-year-old woman with coronary heart disease (CHD) who presented with increasing angina on exertion in 1995, at the age of 45. She suffered from a heterozygous familial hypercholesterolemia and in 1985 her total cholesterol (TCHO) was 328±62 mg/dl (mean value of ten analysis). After ten years of statins her mean values (20 analysis, 2 per year) were: TCHO 259±71, LDL 209±47, HDL 35±7 mg/dl. Coronary angiography (CA) performed in 1995 disclosed three vessel coronary heart disease with significant stenoses of the distal right coronary artery, multiple calcifications of the interventricularis artery and multiple plaques with significant stenoses in the ramus circumflexus. The woman underwent coronary by-pass surgery. Thereafter the patient was treated for six years with HELP in biweekly intervals, in combination with statins. TCHO, LDL, HDL and fibrinogen (fb) levels were measured before and after each treatment. Their mean values for an amount of 120 sessions were: TCHO pre 216±23, post 111±18 LDL pre 152±16 post 67±18, HDL pre 42±5 post 35±4 fb pre 306±48 post 125±31. In 2001 a new CA was performed. Calcifications disappeared and stenoses were identical to the previous CA or reduced. There were no further clinical manifestations of CHD. We trust that the clinical benefit of the HELP procedure will be substantial for those patients who have problems in clearing LDL from their plasma pool and who are at the same time sensitive to elevated LDL levels by the development of premature coronary sclerosis.

PLoS ONE ◽  
2018 ◽  
Vol 13 (7) ◽  
pp. e0200017 ◽  
Author(s):  
Peter Ueda ◽  
Pablo Gulayin ◽  
Goodarz Danaei

2002 ◽  
Vol 18 (3) ◽  
pp. 121-128 ◽  
Author(s):  
Adelheid Schwarz ◽  
Werner Haberbosch ◽  
Harald Tillmanns ◽  
Andreas Gardemann

Background.Matrix metalloproteinases, such as stromelysin-1, are implicated in the pathogenesis of coronary artery disease (CAD) and acute myocardial infarction (MI). A 5A/6A promoter polymorphism can regulate the transcription of the stromelysin-1 gene in an allele-specific manner. Evidence has been presented that the 6A allele is associated with the progression of coronary heart disease (CHD). In contrast, the 5A allele may be linked to the risk of MI.Results.To analyse the relation of the 5A/6A polymorphism with the risk and severity of CHD and the risk of MI, a case-control study of 515 healthy controls and 1848 participants who underwent coronary angiography for diagnostic purposes was conducted. In the total sample, the mean CHD scores—according to Gensini—were different between 5A/6A genotypes: 5A5A homozygotes had the lowest, 6A6A genotypes the highest and 5A6A heterozygotes intermediate scores. These differences were even more pronounced when the participants were restricted to individuals with a high coronary risk profile (high apoB levels, high Lp(a) levels, high glucose levels, combinations of either high apoB and Lp(a) levels or high apoB, Lp(a) and glucose plasma levels). Mean values were used as cut points for high-risk populations, respectively. In contrast, the 5A allele was not associated with the risk of CHD or MI. Even when angiographically controlled individuals without MI were compared with MI patients in subpopulations of participants with no, single, double and triple vessel disease, the frequencies of the 5A/6A and/or the 5A5A genotypes were not higher in each subgroup, respectively.Conclusions.The present results do not confirm an association of the 5A allele with the risk of MI, observed in another investigation, but strengthen the hypothesis of earlier studies that the 6A allele is a disease marker for progression of coronary heart disease. Further investigations should evaluate whether 6A allele carriers and especially 6A homozygotes might benefit from a more aggressive therapy against CHD progression.


2005 ◽  
Vol 41 (1) ◽  
pp. 219-225 ◽  
Author(s):  
Kristina Sundquist ◽  
Jan Qvist ◽  
Sven-Erik Johansson ◽  
Jan Sundquist

2020 ◽  
Vol 13 (6) ◽  
pp. 33-37
Author(s):  
OLGA B. OSHCHEPKOVA ◽  
◽  
EVGENY V. ARKHIPOV ◽  
GULNAZ M. MUKHAMETGALIEVA ◽  
OLGA YU. MIKHOPAROVA ◽  
...  

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