Gender differences in acute coronary syndromes: Do they count?

Aim: INTRODUCTION: We investigated the different control of cardiovascular risk factors such as total cholesterol, LDL, HDL, apolipoprotein A, apolipoprotein B, apolipoprotein B/A1 ratio and Lp (a) at the onset of atherosclerotic disease in male and females. Methods: We consecutively enrolled 539 patients admitted to our Coronary Care Unit (CCU) with diagnosis of Acute Coronary Syndrome (ACS) (STEMI, NSTEMI, Unstable Angina) confirmed by a coronary angiography showing obstructive lesions (> 75%). We then divided this population into two groups: 1 (men) and 2 (women). Results: In the sample analyzed, 77% of patients are men and 23% women. Women are older than men at the onset of ischemic heart disease or during relapse. Probably because older,women are more often hypertensive (83% vs 63%), diabetics and with an impaired renal function. There were no significant differences in the values of total cholesterol, LDL and apolipoprotein B. In women, triglyceride values are lower than men (133 mg / dl vs. 151 mg / dl), while those of HDL are generally higher (46 mg / dl vs. 39 mg / dl). In women, the levels of apoA1 are higher (125 mg / dl vs. 111 mg / dl) and consequently the ratio apolipoprotein B / apolipoprotein A1 (0.81 vs 0.97) appears to be lower. The plasma levels of Lp (a) were elevated in 37% of the total population and especially in women, in which the average concentration is about 40 mg / dl: the difference between the genders was not statistically significant. Conclusion: From our data it appears that the distribution of risk factors for ACS is dependent on sex and that, in light of the different post ACS prognosis, in certain subpopulations of patients, can be taken in consideration different treatment strategies

Recurrence of acute coronary syndrome during inadeguate control of cardiovascular risk factors

It is recognized that inadeguate control of cardiovascular risk factors is involved in the onset and progression of atherosclerotic diseases. In particular, data indicate that inadequate reduction of total cholesterolemia, LDL and HDL values, achieved by pharmacological and non pharmacological methods, implicates a raised risk of new events. By contrast, it is not clearly acknowledged the role played by other risk factors, as Apolipoprotein A, Apolipoprotein B, Apolipoprotein B/A1 ratio and Lipoprotein (a).Methods: We analyzed data from 539 consecutively recruited subjects affected by Acute Coronary Syndrome (STEMI, NSTEMI, Unstable Angina) confirmed by critical obstructive lesions at Coronary Angiography. The patients, admitted at our Coronary Care Unit (CCU), were divided in two groups: Group 1(first event), Group 2 (recurrence). Results: In our population an ischaemic recurrent event was more frequently NSTEMI (59% vs 28%) or Unstable Angina (14% vs 7%), rather than STEMI and it was more common in the elderly (69 yrs vs 63 yrs), in overweight patients, in hypertensives (88% vs 57%) and in diabetics (38% vs 27%) Addictionally, patients of Group 2 vs Group 1 presented an insufficient control of dyslipidemia, with not optimal level of total cholesterol (159 vs 185 mg/dl), LDL cholesterol (99 vs 122mg/dl), apolipoprotein B (93 vs 108 ng/dl), Lipoprotein (a) (41 vs 30 mg/dl) and Apolipoprotein B/A1 ratio (0,86 vs 0,97). Patients of Group 1 were often naive from a therapeutical point of view, not taking any medications for hypertension, dyslipidemia and therefore they had very often an even worse control of risk factors rather than Group 2. Surprisingly we noticed that 40% of patients of Group 2 were not compliant to hypolipidemic therapy, thus resulting in LDL cholesterol level not at target following international Guidelines (<70 mg/dl) in most of them (77%). Addictionally,Group 2 subjects had more frequently a multi-vessel coronary artery disease (75% vs 55%)and a reduced renal function (GFR: 73 ml/min vs 84 ml/min). Conclusion: Therefore, our data suggest that in Coronary Artery Disease risk factors control result suboptimal both in primary and in secondary prevention

Plasmatic and phenotypic effects with alirocumab, a PCSK9 inhibitor, in familial hypercholesterolemia treatment (FH)

Aim: FH therapy is based on HMG-CoA reductase inhibitors, Ezetimibe and apheresis. Recently, PCSK9 antagonists were introduced as an "add-on therapy" for severe hypercholesterolemia "resistant" to common therapies. Results: Patient 1 had arcus cornealis and tendinous xanthomata and premature CAD. Basal total cholesterol was 433 mg/dl, LDL-C mg/dl 364, triglicerides 180 mg/dl, HDL 31 mg/d, Lp(a) 95 mg/dl. Despite Atorvastatin (80 mg) and Ezetimibe (10 mg), LDL-C level was elevated (180 mg/dl). DLCN was 12. With Alirocumab (75 mg/ml) every 2 weeks, LDL-C reduced to 85 mg/dl. We doubled Alirocumab posology to 150 mg/dl twice a month. Xanthomata were significantly reduced, such as total and LDL cholesterol. Ă Patient 2 had premature CAD and lower limb arteries disease; DLCN score was 5. Despite Atorvastatin (40 mg) and Ezetimibe 10, total cholesterol was 217 mg/dl, LDL-C was not at goal (120 mg/dl). We added Alirocumab (75 mg/ ml) every 2 weeks. Total and LDL-C resulted notably decreased (LDL 3,6 mg/dl). Ezetimibe was discontinued and Atorvastatin reduced. Patient referred reduction of muscular pain after statin dosage reduction and the beginning of regular exercise. Patient 3 had premature CAD, LDL-C (222 mg/dl); despite Torvast 40 mg, Ezetimibe 10 mg and Esapent, we added Alirocumab 75 mg/ml twice a month with LDL-C reduction (54 mg/dl). No untoward effects were reported by the patients. Conclusions: Our group demonstrates a great interindividual variability to response to Alirocumab and regression of skin lipid lesions, never been observed during therapy with statins or other lipid-lowering treatments

Lipoprotein (a) is related to coronary atherosclerotic burden and a vulnerable plaque phenotype in angiographically obstructive coronary artery disease

Background: Lipoprotein Lp(a) has been shown to be an independent risk factor for coronary artery disease (CAD). However, its association with CAD burden in patients with ACS is largely unknown, as well as the association of Lp(a) with lipid rich plaques prone to rupture. Aim: We aim at assessing CAD burden by coronary angiography and plaque features including thin cap fibroatheroma (TCFA) by optical coherence tomography (OCT) in consecutive patients presenting with acute coronary syndrome (ACS) and obstructive CAD along with serum Lp(a) levels. Methods: This study comprises an angiographic and an OCT cohort. A total of 500 ACS patients (370 men, average age 66 +/- 11) were enrolled for the angiographic cohort and 51 ACS patients (29 males, average age 65 +/- 11) were enrolled for the OCT cohort. Angiographic CAD severity was assessed by Sullivan score and by Bogaty score including stenosis score and extent index. OCT plaque features were evaluated at the site of the minimal lumen area and along the culprit segment. Results: In the angiographic cohort, at multivariate analysis, Lp(a) was a weak independent predictor of Sullivan score (p < 0.0001), stenosis score (p < 0.0001) and extent index (p < 0.0001). In the OCT cohort, patients with higher Lp(a) levels (-30 md/ dl) compared to patients with lower Lp(a) levels (< 30 md/ dl) exhibited a higher prevalence of lipidic plaque at the site of the culprit stenosis (67% vs. 27%; P = 0.02), a wider lipid arc (135 +/- 114 vs 59 +/- 111; P = 0.03) and a higher prevalence of TCFA (38% vs. 10%; P = 0.04)

Data on the lipoprotein (a), coronary atherosclerotic burden and vulnerable plaque phenotype in angiographic obstructive coronary artery disease

Lipoprotein Lp(a) represents an independent risk factor for coronary artery disease (CAD). However, its association with CAD burden and lipid rich plaques prone to rupture in patients with acute coronary syndrome (ACS) still remains unknown. These data aim to investigate the association among serum Lipoprotein(a) (Lpa) levels, coronary atherosclerotic burden and features of culprit plaque in patients with ACS and obstructive CAD. For his reason, a total of 500 ACS patients were enrolled for the angiographic cohort and 51 ACS patients were enrolled for the optical coherence tomography (OCT) cohort. Angiographic CAD severity was assessed by Sullivan score and by Bogaty score including stenosis score and extent index, whereas OCT plaque features were evaluated at the site of the minimal lumen area and along the culprit segment. In the angiographic cohort, Lp(a) was a weak independent predictor of Sullivan score (p30 md/dl) compared to patients with lower Lp(a) levels (<30 md/dl) exhibited a higher prevalence of lipidic plaque at the site of the culprit stenosis (P=0.02), a wider lipid arc (p=0.003) and a higher prevalence of thin-cap fibroatheroma (p=0.004)