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    Complementary and Alternative Medical Lab Testing Part 3: Cardiology
    Complementary and Alternative Medical Lab Testing Part 3: Cardiology
    Complementary and Alternative Medical Lab Testing Part 3: Cardiology
    Ebook334 pages4 hours

    Complementary and Alternative Medical Lab Testing Part 3: Cardiology

    By Ronald Steriti

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    About this ebook

    Complementary and Alternative Medical Lab Testing (CAM Labs) contains summaries of the published research on lab tests, primarily from PubMed trials on humans. Each chapter (disease) begins with a brief summary of conventional lab tests, followed by additional lab tests, including diabetes, insulin resistance, metabolic syndrome, inflammation, etc. There are sections on endocrine hormones (thyroid, adrenal, sex steroids) and environmental medicine (toxic heavy metals). The nutritional assessments section includes minerals, vitamins and amino acids.

    CAM Labs 3 – Cardiology

    1. Aneurysm
    2. Angina
    3. Arrhythmia
    4. Atrial Fibrillation
    5. Cardiac Syndrome X
    6. Cardiomyopathy
    7. Congestive Heart Failure
    8. Coronary Artery Disease
    9. Hypertension
    10. Hypertension, Resistant
    11. Myocardial Infarction
    12. Myocarditis
    13. Stroke
    14. Syncope
    15. Ventricular Tachycardia

    Cardiac Labs
    16. Homocysteine
    17. Hypercholesterolemia
    18. Hypertriglyceridemia
    19. Low HDL (Hypoalphalipoproteinemia)

    LanguageEnglish
    PublisherRonald Steriti
    Release dateJun 4, 2016
    ISBN9781311060570
    Complementary and Alternative Medical Lab Testing Part 3: Cardiology
    Author

    Ronald Steriti

    Dr. Ronald Steriti is a graduate of Southwest College of Naturopathic Medicine and currently is researcher for Jonathan V. Wright at the Tahoma Clinic.

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      Complementary and Alternative Medical Lab Testing Part 3 - Ronald Steriti

      Chapter 1. Aneurysm

      An aneurysm occurs when part of a blood vessel (artery) or cardiac chamber swells (dilates). This can be caused when either the blood vessel is damaged, or there is a weakness in the wall of the blood vessel. As blood pressure builds up the blood vessel balloons out at its weakest point.

      Conventional Lab Tests

      CBC with platelets

      Prothrombin time (PT)/activated partial thromboplastin time (aPTT)

      Serum chemistries, including electrolytes and osmolarity

      Additional Lab Tests

      Fasting Glucose, Hemoglobin A1C

      A meta-analysis found a protective role for diabetes on the development of abdominal aortic aneurysm (AAA). The prevalence of diabetes mellitus in studied patients with AAA ranged from 6% to 14%. The prevalence of diabetes in control patients without AAA ranged from 17% to 36%. Pooled analysis suggested a reduced rate of diabetes amongst people with AAA compared to those without (OR 0.65, 0.60-0.70, p<0.001). (Shantikumar et al., 2010)

      Insulin Resistance, Metabolic Syndrome

      A prospective study examined 3196 patients with a history or recent diagnosis of clinically manifest vascular disease. National Cholesterol Education Program (NCEP) and revised NCEP (NCEP-R)-defined Metabolic Syndrome were related to increased risk of vascular events (HR 1.50, 95% CI 1.22-1.84; and 1.50, 1.22-1.87) and all-cause mortality (HR 1.49, 1.20-1.84 and 1.43, 1.14-1.78). Results were similar in the 2472 patients without type 2 diabetes (DM2) and localization of vascular disease; SBP-category (<140 or > or =140 mmHg) or LDL-category (<2.5 or > or =2.5 mmol/L) did not affect this relation. (Wassink et al., 2008)

      This cross-sectional survey of 1117 patients, aged 18-80 years, mean age 60+/-10 years, comprised patients with coronary heart disease (n=527), cerebrovascular disease (n=258), peripheral arterial disease (n=232) or abdominal aortic aneurysm (n=100). Metabolic syndrome was defined by Adult Treatment Panel III. The prevalence of the metabolic syndrome in the study population was 46%: 58% in PAD patients, 41% in CHD patients, 43% in CVD patients and 47% in AAA patients. (Gorter et al., 2004)

      The study population of this cross-sectional survey consisted of 502 patients recently diagnosed with coronary heart disease (CHD), 236 with stroke, 218 with peripheral arterial disease (PAD) and 89 with abdominal aortic aneurysm (AAA). Metabolic syndrome was diagnosed according to Adult Treatment Panel III criteria. The prevalence of the metabolic syndrome in the study population was 45%. In PAD patients this was 57%; in CHD patients 40%, in stroke patients 43% and in AAA patients 45%. (Olijhoek et al., 2004)

      C-Reactive Protein (CRP)

      In 435 patients with asymptomatic AAAs followed up in our outpatient department, the median hs-CRP level was 4.23 mg/L. The aorta diameter increased in the four groups of patients determined according to hs-CRP quartiles (35 +/- 2, 40 +/- 3, 49 +/- 4, and 58 +/- 5 mm; P = .01). The median rate of CRP level variation per year was 1.4 mg/L. Patients with an elevation >1.4 mg/L had an expansion rate of 4.8 mm vs 3.9 mm in those <1.4 mg/L (P < .01). The multivariate age-adjusted logistic model confirmed initial diameter and variation of CRP level were the only factors associated with expansion, with odds ratios (95% confidence intervals) of 6.3 (3.1-7.5) and 3.4 (2.1-5.6). (De Haro et al., 2012)

      In 39 patients with AAA the mean (SD) hsCRP was 3.23 (2.96) mg/L. After log-transformation, hsCRP correlated significantly with aneurysmal size (r=0.477, P=0.002). When the patients were divided into 3 equally sized groups according to hsCRP level, aortic diameter increased from lowest to upper hsCRP-tertile (49 mm, 61 mm, and 67 mm, respectively; P<0.05 for 3rd versus 1st tertile). This association persisted after correction for risk factors. (Vainas et al., 2003)

      Comprehensive Sex Steroid Panel

      Testosterone and LH in Men

      A cross-sectional analysis included 3620 community-dwelling men aged 70-88 yr. AAA (aortic diameter > or =30 mm) was present in 262 men (7.2%). Men with AAA had lower serum total and free testosterone (mean +/- sd 14.5 +/- 6.0 vs. 15.5 +/- 5.6 nmol/liter, P = 0.005 and 256 +/- 87 vs. 280 +/- 97 pmol/liter, P < 0.001, respectively) compared with men without. LH was higher in men with AAA (median, interquartile range: 4.9, 3.1-7.9 vs. 4.3, 3.0-6.4 IU/liter, P = 0.013). In multivariate analysis adjusting for potential confounders, free testosterone was negatively associated with AAA (odds ratio per 1 sd increase: 0.84, 95% confidence interval 0.72-0.98, P = 0.026). LH was positively associated (odds ratio 1.14, 95% confidence interval 1.03-1.25, P = 0.008). Comparable results were seen with aortic diameter analyzed as a continuous variable. (Yeap et al., 2010)

      Estrogen

      In the pathogenesis of AAA, estrogen may play an inhibitory role by decreasing expression of MMP-2 and MMP-9 synthesis. (Wu et al., 2009)

      Aromatase

      The protective effect of female gender on AAAs is due to estrogen synthesis and requires the presence of both ovarian and extragonadal/peripheral aromatase. Peripheral estrogen synthesis accounts for roughly half of the protective effect of female gender. (Johnston et al., 2014)

      Nutritional Assessments

      Copper and Magnesium

      Relationship between concentration of Mg and Cu in serum and the arterial wall was studied in patients with atherosclerosis obliterans (AO), aortic aneurysm (AA) and in the control group. The effect of ageing was also evaluated. The results showed increased serum concentration of Cu in the eldest control group (50-59 years) when compared to the younger (20-29 years). Serum concentration of Mg was decreased in AO and AA, and that in the arterial wall was lower in AA, than in controls. Concentration of Cu in serum and the arterial wall was higher in AO than in controls. Lower limb ischaemia results in decreased serum Mg and increased Cu in the critical degree as compared with the moderate degree of ischaemia. The ratio Mg/Cu was found lower both in serum and the arterial wall in AO and AA, as a result of ageing and vascular disease, and it could be better marker of ischaemia than individual element concentrations. (Iskra et al., 2002)

      Homocysteine

      A meta-analysis of observational studies that evaluated Hcy levels in subjects with AAA compared to unaffected controls analyzed 7 studies with 6,445 participants. Overall, elevated plasma Hcy was associated with an increased risk of AAA (3.29; 95% CI 1.66-6.51). The pooled adjusted OR from a random effect model of only men participants in the AAA compared with the control group was 2.36 (95% CI 0.63-8.82). (Cao et al., 2014)

      A recent study found that elevated tHcy is associated with the presence of AAA in older men. There is also a positive dose-response relationship between tHcy and abdominal aortic diameter. OR was 1.45 (95% CI, 1.10-1.91). Every 5-mumol/L increment in tHcy was associated with 0.15-mm (95% CI, 0.01-0.28 mm) increase in mean aortic diameter. (Wong et al., 2013)

      Vitamin B6 (P5P)

      Patients with a history of AAA were recruited from the outpatient clinic; 60% had already undergone surgery for their AAA. They were asked to invite a friend or neighbor to participate as a control subject (age-matched and sex-matched). Univariate analysis showed an odds ratio (OR) of 2.2 (95% confidence interval (CI), 0.9 to 5.5) for the risk of AAA for the highest quartile of homocysteine concentration. After adjustment for creatinine, the OR was markedly reduced to 1.24 (95% CI, 0.42 to 3.66), and this risk further attenuated in the multivariate analysis. Univariate analysis of the B vitamins showed an increased risk of AAA for the bottom quartile of vitamin B6 (OR, 3.75; 95% CI, 1.22 to 11.54), which even increased after adjustments. (Peeters et al., 2007)

      Vitamin E

      Three groups of male patients were screened: (1) patients undergoing elective operative repair of AAA reaching more than 4.5 cm in transversal diameter (AAA group, n = 19, mean age 72.5 +- 6.6 years), (2) atherosclerotic patients referred to our department for coronary bypass artery surgery (CAB group, n = 18, mean age 61.2 +- 7.4 years), and (3) healthy volunteers (healthy volunteers group, n =13, mean age 35.2 +- 16.3 years). The plasma vitamin E level was below sensitivity limit (<0.6 pg/mL plasma) in 6 of 19 patients of the AAA group. In this group, the mean value of vitamin E concentration reached 1.63 +- 2.44 pg/mL plasma. This value was significantly lower than the plasma vitamin E levels observed in the CAB group (11.00 +- 4.79 Fg/mL, p < 0.001) and in the healthy volunteers group (10.90 +- 3.12 pg/mL, p < 0.001). Similarly, the vitamin E/total lipid ratio was significantly lower in the AAA group (0.26 +- 0.37 mg/g) versus the CAB group (2.51 +- 1.6 mg/g, p < 0.001), and the healthy volunteers group (2.01 +- 0.47 mg/mL, p < 0.001). (Sakalihasan et al., 1996)

      Vitamin B12

      A recent study examined 119 patients with AAA and 36 controls without aneurysm matched by age, gender and smoking habit. The present study shows a significant inverse correlation between maximum diameter of the non-ruptured AAA (n=78) and B12 (r = -0.304, p=0.007) with significant higher levels in small AAA compared to large AAA. (Lindqvist et al., 2012)

      Vitamin B12 and Homocysteine

      A case control study included 38 AAA patients and 36 controls. Twenty-six (68%) of the AAA patients had elevated levels of homocysteine compared to 2 (6%) in the case control group. The mean homocysteine level in the AAA group was 19.4 micromol/L (SE +/- 1.1) (95% CI 17.17-21.65) and in the control group was 10.9 micromol/L (SE +/- 1) (95% CI 9.95-11.88) (p<0.001). Mean vitamin B12 level in the AAA and the controls was 332.11 pg/L (SE +/- 16.44) and 414.33 pg/L (SE +/- 19.72), respectively (p<0.004). Mean folic acid in the AAA was 8.02 (SE +/- 0.71) and the control was 9.8 etagm/L (SE +/- 0.69), (ns). (Warsi et al., 2004)

      References

      Cao, H., et al. (2014), ‘Homocysteine level and risk of abdominal aortic aneurysm: a meta-analysis’, PLoS One, 9 (1), e85831. PubMedID: 24465733

      De Haro, J., et al. (2012), ‘Prediction of asymptomatic abdominal aortic aneurysm expansion by means of rate of variation of C-reactive protein plasma levels’, J Vasc Surg, 56 (1), 45-52. PubMedID: 22551908

      Gorter, P. M., et al. (2004), ‘Prevalence of the metabolic syndrome in patients with coronary heart disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm’, Atherosclerosis, 173 (2), 363-69. PubMedID: 15064114

      Iskra, M., W. Majewski, and M. Piorunska-Stolzmann (2002), ‘Modifications of magnesium and copper concentrations in serum and arterial wall of patients with vascular diseases related to ageing, atherosclerosis and aortic aneurysm’, Magnes Res, 15 (3-4), 279-85. PubMedID: 12635884

      Johnston, W. F., et al. (2014), ‘Aromatase is required for female abdominal aortic aneurysm protection’, J Vasc Surg, PubMedID: 24582702

      Lindqvist, M., A. Hellstrom, and A. E. Henriksson (2012), ‘Abdominal aortic aneurysm and the association with serum levels of Homocysteine, vitamins B6, B12 and Folate’, Am J Cardiovasc Dis, 2 (4), 318-22. PubMedID: 23173106

      Olijhoek, J. K., et al. (2004), ‘The metabolic syndrome is associated with advanced vascular damage in patients with coronary heart disease, stroke, peripheral arterial disease or abdominal aortic aneurysm’, Eur Heart J, 25 (4), 342-48. PubMedID: 14984924

      Peeters, A. C., et al. (2007), ‘Low vitamin B6, and not plasma homocysteine concentration, as risk factor for abdominal aortic aneurysm: a retrospective case-control study’, J Vasc Surg, 45 (4), 701-5. PubMedID: 17398378

      Sakalihasan, N., et al. (1996), ‘Decrease of plasma vitamin E (alpha-tocopherol) levels in patients with abdominal aortic aneurysm’, Ann N Y Acad Sci, 800 278-82. PubMedID: 8959014

      Shantikumar, S., et al. (2010), ‘Diabetes and the abdominal aortic aneurysm’, Eur J Vasc Endovasc Surg, 39 (2), 200-7. PubMedID: 19948418

      Vainas, T., et al. (2003), ‘Serum C-reactive protein level is associated with abdominal aortic aneurysm size and may be produced by aneurysmal tissue’, Circulation, 107 (8), 1103-5. PubMedID: 12615785

      Warsi, A. A., et al. (2004), ‘Abdominal aortic aneurysm and its correlation to plasma homocysteine, and vitamins’, Eur J Vasc Endovasc Surg, 27 (1), 75-79. PubMedID: 14652841

      Wassink, A. M., et al. (2008), ‘Metabolic syndrome and the risk of new vascular events and all-cause mortality in patients with coronary artery disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm’, Eur Heart J, 29 (2), 213-23. PubMedID: 18199567

      Wong, Y. Y., et al. (2013), ‘Plasma total homocysteine is associated with abdominal aortic aneurysm and aortic diameter in older men’, J Vasc Surg, 58 (2), 364-70. PubMedID: 23643559

      Wu, X. F., et al. (2009), ‘The role of estrogen in the formation of experimental abdominal aortic aneurysm’, Am J Surg, 197 (1), 49-54. PubMedID: 18585678

      Yeap, B. B., et al. (2010), ‘Associations of total testosterone, sex hormone-binding globulin, calculated free testosterone, and luteinizing hormone with prevalence of abdominal aortic aneurysm in older men’, J Clin Endocrinol Metab, 95 (3), 1123-30. PubMedID: 20061425

      Chapter 2. Angina

      Angina is a symptom complex resulting from mismatch of myocardial oxygen demand and supply.

      Conventional Lab Tests

      CBC

      Creatine phosphokinase (CPK) and creatine kinase (CK)

      Troponin I and T (TnI and TnT).

      Total cholesterol, HDL, LDL, and triglycerides

      Additional Lab Tests

      Insulin and IL-6

      The study included 50 patients with unstable angina divided into a female group that contained 16 female patients with an age range of 35-73 years, and a male group that contained 34 male patients with an age range of 40-72 years. Control groups contained forty healthy individuals. The levels of insulin and IL-6 were considerably elevated throughout (p < 0.001), an optimistic relationship concerning insulin with CRP and IL-6 in unstable angina patients. There was increase in the level of insulin regarding patients with unsteady angina as a result of insulin resistance that was caused by the elevated level of pro-inflammatory cytokine (IL-6). (Al-Karkhi et al., 2013)

      Insulin Resistance, Metabolic Syndrome

      The study participants include 111 coronary spastic angina (CSA) patients (81 men and 30 women, mean age 62+/-12 years) and 53 participants without CSA (24 men and 29 women, mean age 63+/-10 years), serving as the controls. The number of men, the number of smokers, log post-glucose-IR, the insulin sensitivity index, and fasting plasma glucose levels were higher in CSA patients compared with controls (P=0.001, 0.001, 0.004, 0.012, and 0.013, respectively), whereas plasma high-density lipoprotein cholesterol levels were lower (P<0.001). (Kashiwagi et al., 2013)

      A total of 265 selected patients with vasospastic angina (VSA) and 56 control subjects with atypical chest pain were enrolled in the present study. During the median follow-up period of 90.0 months, thirty-one patients developed cardiac events, including 6 sudden cardiac deaths and 25 readmissions for acute coronary syndrome. Cardiac events occurred in 38.9% of the patients with an IRI 120 >/= 80 muU/ml and only 1.6% of the patients with an IRI 120<80 muU/ml (log rank 77.220, p<0.001). A multivariate analysis showed that an IRI 120 >/= 80 muU/ml (hazard ratio 27.49, 95% confidence interval: 4.66-162.10, p<0.001) was an independent predictor of cardiac events. These data indicate that insulin resistance associated with compensatory hyperinsulinemia increases the risk of cardiac events in VSA patients. (Nakagomi et al., 2013)

      100 consecutive non-diabetic patients with stable CAD referred to coronary angiography were studied. After OGTT, 44% of patients presented disturbed glucose metabolism: 9% of patients had newly diagnosed diabetes and 35% patients were in the pre-diabetic state. Abnormal glucose regulation is very common in patients with stable CAD. (Wlodarczyk and Strojek, 2008)

      The study population consisted of 60 patients with VAP and 42 control subjects (62 subjects with normal glucose tolerance and 40 with impaired glucose tolerance). Compared with the control group, the 2-hour insulin area (area under the plasma insulin concentration-time curve) during a 75-g oral glucose tolerance test was significantly higher in both VAP groups with normal and impaired glucose tolerance. A high frequency of vasospastic angina was observed in subjects with clustered risk factors for insulin resistance syndrome, suggesting a close association of VAP with this syndrome. In stepwise discriminant analysis, the 2-hour insulin area was significantly associated with VAP independent of other risk factors. SSPG level in VAP was about twofold over control, indicating the presence of insulin resistance in patients with VAP. (Shinozaki et al., 1995)

      C-Reactive Protein (CRP)

      The study population comprised of 311 consecutive patients with chronic stable angina (SA) who underwent coronary stent implantation on initial admission and angiographic follow-up ((8.5 +/- 1.2) months). Rapid angiographic progression of non-target lesions occurred in 136 patients (43.7%) at follow-up: 77 had a >/= 10% diameter reduction of pre-existing stenosis >/= 50%, 26 had a >/= 30% diameter reduction of a pre-existing stenosis < 50%, 64 developed a new lesion >/= 30% in a previously normal segment, and 4 had progression of a lesion to total occlusion. Progression of non-target lesions was not associated with target lesion restenosis formation. High-sensitive CRP levels were markedly higher in progression patients than in non-progression ones (1.60 (0.80 - 3.46) mg/L vs. 0.96 (0.55 - 1.87) mg/L, P < 0.001). Multivariate regression analysis showed that plasma CRP independently predicted rapid angiographic progression of non-target lesions (P = 0.001). High-sensitive CRP levels above 1.32 mg/L (the cutoff value) were associated with a 3.5-fold increase in the risk of developing rapid atherosclerotic progression (OR = 3.497, 95%CI 2.045 - 5.980). (Xu et al., 2011)

      In this analytical cross sectional study which was conducted in 2007 in Chamran hospital, samples were collected using simple sampling and included 80 patients who referred to the hospital due to angina pectoris, had the diagnosis of unstable angina and were candidates of angiography. Mean level of CRP in the population under study was 6.05 +/- 4 mg/dl which was 1.37 +/- 2 and 8.01 +/- 6 in simple and complex groups respectively (P < 0.05). CRP mean was significantly higher in the group with complex lesions, less than 1 mg/dl in simple lesion and more than 4 mg/dl in complex lesions. (Sadeghi et al., 2010)

      A prospective study included 291 patients referred for coronary angiography due to clinically suspected stable angina pectoris (SAP). The primary outcome was predefined as death from any cause, myocardial infarction or stroke during a mean follow-up of 7.1 years. Thirty four patients experienced the primary outcome. Hazard ratios and 95% confidence intervals for the primary outcome were: sVCAM-1: 2.4 (1.1-4.9), sICAM-1: 3.3 (1.5-7.2), sP-selectin: 1.2 (0.6-2.6] and hs-CRP: 3.1 (1.5-6.3), when comparing patients in the 4th quartile with those in lower quartiles in a multivariable model. Higher risk of adverse outcome was observed in patients having levels of both hsCRP and sICAM-1 (HR 4.7, 1.7-9.9) or hsCRP and sVCAM-1 (HR 4.2, 1.7-9.9) in the 4th quartile. sVCAM-1, sICAM-1 and hsCRP were significantly associated with long term outcomes of patients with SAP beyond the risk associated with traditional risk factors. (Eschen et al., 2010)

      Fibrinogen and CRP

      In a substudy of the prospective AtheroGene registry, we assessed in 1806 patients with documented CAD and stable angina pectoris, the risk of cardiovascular death and non-fatal myocardial infarction (n=183) over a median follow-up of 3.5 (maximum 7.7) years. C-reactive protein and fibrinogen were associated with future cardiovascular events, such as an increment in one standard deviation of C-reactive protein is associated with a 1.15-fold (95% CI 1.05-1.27, P=0.002) increase, an increment of one standard deviation of fibrinogen with a 1.27-fold (95% CI 1.12-1.43, P<0.0005) increase in hazard risk in the models adjusted for age and sex. (Sinning et al., 2006)

      Lipoprotein (a) and CRP

      A study examined 49 apparently healthy men and women, 82 patients having stable angina pectoris (SAP), 80 patients with unstable angina (USAP), and 106 patients with acute ST-elevation myocardial infarction (STEMI) treated or not treated with statins. CRP showed the best ROC characteristics in the assessment of STEMI patients. Lp(a) is better in the evaluation of SAP and USAP patients, considering that Lp(a) showed the highest area under the curve (AUC). (Djordjevic et al., 2011)

      Apolipoprotein A1 and CRP

      A group of patients with stable angina contained 295 patients (217 males and 78 females) with a mean age of 65.69+/-11.24 years. Arithmetic and geometric means of C-reactive protein in the sample were 10.7 and 1.4 mg/l, respectively. Distributing the sample by quartiles of C-reactive protein, we found a positive correlation between C-reactive protein, fibrinogen and D-dimer levels (p<0.000), and an inverse correlation for HDL cholesterol and apolipoprotein A1 (p<0.000). In multivariate analysis, fibrinogen (p<0.000) and D-dimer (p<0.01) levels were independently associated with high levels of C-reactive protein. Of the lipid factors, only apolipoprotein A1 (p<0.000) was independently and inversely associated with high levels of C-reactive protein. (Sagastagoitia et al., 2007)

      Platelet-Lymphocyte Ratio (PLR>138)

      A total of 294 patients with both stable angina pectoris (SAP) and chronic total occlusion (CTO) were classified according to their Rentrop collateral grades as either poor (Rentrop grades/0-1) or good (Rentrop grades/2-3). The PLR values were significantly higher in patients with poor coronary collateral circulation (CCC) than in those with good CCC (156.8 + 30.7 vs 132.1 + 24.4, P<0.001). In regression analysis, PLR (unit=10) (OR 1.48, 95% CI 1.33 -1.65; P<0.001) and high-sensitivity C-reactive protein were found to be the independent predictors of poor CCC. In receiver operator characteristic curve analysis, optimal cut-off value of PLR to predict poor CCC was found as 138.1, with 76% sensitivity and 65% specificity. PLR may be an important, simple, and cost effective tool predicting the degree of collateralization in patients with SAP and CTO. (Acar et al., 2013)

      Comprehensive Sex Steroid Panel

      Estrogen in Women

      A study examined nine premenopausal women, mean (SEM) age 38.89 (2.18) years, with established coronary heart disease, symptomatic angina, and a positive exercise test. The early follicular phase, when estradiol and progesterone concentrations were both low, was associated with the worst exercise performance in terms of time to onset of myocardial ischaemia, at 290 (79) seconds; the best performance (418 (71) seconds) was when oestrogen concentrations were highest in the mid-cycle (p < 0.05). Similar trends were observed in other measured variables. Progesterone concentrations did not influence exercise performance. During the menstrual cycle myocardial ischemia was more easily induced when estrogen concentrations were low. (Lloyd et al.,

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