|Year : 2016 | Volume
| Issue : 1 | Page : 20-26
Troponin I as marker of subclinical cardiac injury in human immunodeficiency virus-seropositive patients in Sokoto, Nigeria
Aminu Bello1, Abdullah S Mainasara1, Hamidu M Liman2, Umar Hayatu2, Abdullahi F Abubakar1, Kasimu Saidu1, Bashar Sani3, Aminu A Umar4
1 Department of Chemical Pathology and Immunology, Faculty of Basic Medical Sciences, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria
2 Department of Internal Medicine, Faculty of Clinical Sciences, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria
3 Department of Chemical Pathology, Usmanu Danfodiyo University Teaching Hospital, Sokoto, Nigeria
4 Department of Morbid Anatomy and Forensic Medicine, Faculty of Basic Medical Sciences, College of Health Sciences, Usmanu Danfodiyo University, Sokoto, Nigeria
|Date of Web Publication||13-Jul-2017|
Department of Chemical Pathology and Immunology, Faculty of Basic Medical Sciences College of Health Sciences, Usmanu Danfodiyo University, Sokoto
Source of Support: None, Conflict of Interest: None
INTRODUCTION: Myocardial injury remains a challenging health issue among human immunodeficiency virus (HIV)/acquired immuno deficiency syndrome patients, and the importance for the estimation of cardiac troponin I (cTnI) as a tool for early detection of cardiac injury has been proven by many studies. This study examined the specificity of cTnI estimation and other cardiac enzymes in detection of subclinical cardiac injury in HIV-positive patients.
MATERIALS AND METHODS: One hundred and forty patients and 70 controls between the ages of 15–80 years were studied. The patients were grouped into three categories: seventy patients on highly active antiretroviral therapy (HAART), seventy on HAART-naïve patients, and seventy were recruited as controls.
RESULTS: The values (mean ± standard error of mean) of cTnI, total creatine kinase (TCK), creatine kinase muscle and brain subtype (CKMB), and lactate dehydrogenase (LDH) in patients on HAART were 3.32 ± 0.32 ng/mL, 83.52 ± 9.69 IU/L, 30.79 ± 2.02 IU/L, and 517.4 ± 19.23 IU/L, respectively. For the HAART-naïve patients, the values were 2.37 ± 0.22 ng/mL, 72.53 ± 6.47 IU/L, 51.02 ± 10.86 IU/L, and 439 ± 17.72 IU/L whereas for controls the values were 1.62 ± 0.19 ng/mL, 54.86 ± 5.82 IU/L, 15.60 ± 1.63 IU/L, and 355.30 ± 23.40 IU/L with P values <0.0001, 0.0265, 0.0007, <0.0001 which were statistically significant for cTnI, TCK, CKMB, and LDH, respectively. However, all the parameters studied were found to be elevated in patients than in the controls.
CONCLUSIONS: The study showed that about 121 (86.4%) of studied cases had elevated serum cTnI, of which 65 (53.7%) had elevated serum CKMB which strongly suggested subclinical myocardial injury among majority of the HIV-seropositive patients in this study.
Keywords: Cardiac injury, human immunodeficiency virus, marker, subclinical, troponin I
|How to cite this article:|
Bello A, Mainasara AS, Liman HM, Hayatu U, Abubakar AF, Saidu K, Sani B, Umar AA. Troponin I as marker of subclinical cardiac injury in human immunodeficiency virus-seropositive patients in Sokoto, Nigeria. J HIV Hum Reprod 2016;4:20-6
|How to cite this URL:|
Bello A, Mainasara AS, Liman HM, Hayatu U, Abubakar AF, Saidu K, Sani B, Umar AA. Troponin I as marker of subclinical cardiac injury in human immunodeficiency virus-seropositive patients in Sokoto, Nigeria. J HIV Hum Reprod [serial online] 2016 [cited 2017 Oct 23];4:20-6. Available from: http://www.j-hhr.org/text.asp?2016/4/1/20/210591
| Introduction|| |
Human immunodeficiency virus (HIV) infection is a global public health issue, and cardiovascular disease has been well documented in patients with HIV infection. At present, HIV infection is one of the leading causes of acquired cardiovascular disease including heart failure. Highly active antiretroviral therapy (HAART) has prolonged many patients' lives, but the cardiac sequelae may progress despite HAART. HAART has significantly changed the course of HIV disease, resulting in prolonged survival and improved quality of life, although increased cardiovascular risk has been reported to be associated with this treatment. Changes in the activities of creatine kinase (CK), aspartate transaminases, and lactate dehydrogenase (LDH) were used as diagnostic criteria for the confirmation of suspected acute myocardial infarction (MI) for several decades. However, none of these enzymes is specific for the myocardium though CK distribution in heart muscle rather than other tissues makes it more advantageous over other enzymes. The troponins are proteins found in cardiac and skeletal muscle tissue as products of separate genes. They are located in the myofibril where they regulate the interaction of actin monomers with the myosin heavy chain., Measurement of myocardial damage by newer, highly specific markers of myocardial damage is now possible, including cardiac structural proteins such as Troponin. This marker is not detectable in the serum of normal population and is highly cardiac specific. In the setting of myocardial injury, it is released into the circulation slightly earlier than CK. Data from a previous study indicated that increased cardiac troponin I (cTnI) did not occur despite severe acute and chronic muscle injury even when plasma levels of creatine kinase muscle and brain subtype (CKMB) increased unless concomitant cardiac injury was present.
Three types of troponin exist: troponin I, troponin T, and troponin C. The increase in levels of cardiac muscle isoform of troponin I, in circulation, is highly indicative of myocardial injury., Detectable increases in the biomarkers of cardiac injury are indicative of injury to the myocardium, but elevations are not synonymous with an ischemic mechanism of injury. Therefore, increases in the past and the present are not suggestive of the diagnosis of MI. cTnI has greater sensitivity and specificity than CKMB and detects recent MI of up to 2 weeks duration. However, most studies of cTnI as a marker for myocardial injury have been limited to patients with cardiac, renal, or muscular disorders. The diagnostic significance of cTnI as a cardiac injury marker in the presence of a broad spectrum of other illnesses needs to be elucidated. The recent introduction of cTnT and cTnI into routine daily clinical practice allows for highly accurate, sensitive, and specific determination of myocardial injury, and in the setting of myocardial ischemia, it is now possible to define infarcts of minimal size as well as larger infarcts.
| Materials and Methods|| |
This is a cross-sectional descriptive study which was performed on HIV-seropositive patients attending Usmanu Danfodiyo University Teaching Hospital (UDUTH), Specialist Hospital Sokoto (SHS), and Maryam Abacha Women and Children Hospital (MAWCH) in Sokoto metropolis.
The study population was grouped into three categories. All HIV-seropositive patients receiving HAART medication at UDUTH, SHS, and MAWCH and all HIV-seropositive HAART-naïve patients receiving care at UDUTH, SHS, and MAWCH during the study period were considered eligible for enrolment in the study. HIV-seronegative, age- and sex-matched individuals were considered controls. The number of patients for inclusion in the study was determined using the sample size formula for estimating sample size for descriptive studies. Thus, each group of study population was recruited as follows:
- Seventy HIV-positive HAART-naïve patients
- Seventy HIV-positive patients on HAART
- Seventy age- and sex-matched HIV-negative individuals who were considered controls.
Therefore, a total of 210 individuals were recruited for the study.
Ethical approval was obtained from the Ethics Committees of the Ministry of Health Sokoto State, and UDUTH. Written informed consent was obtained from the participants.
Methods and instruments of data collection
A semi-structured, interviewer-administered questionnaire was used to collect the demographic data and other relevant information from the selected individuals, such as biodata, duration of the disease, duration of therapy, and clinical features (adverse drugs reaction, history of chest pain since diagnosis, and rashes).
HIV screening was carried out using “Determine HIV 1 and 2 test kits,” manufactured by Abbott Laboratories (Tokyo, Japan). Blood pressure (BP) was measured using accus sphygmomanometer England, and body mass index was calculated from the weight and height. Troponin I was analyzed using Troponin I (cTnI) ELISA method from Calbiotech, Life Science Company (CA, USA). Rayto 2100C microplate reader (Rayto Life and Analytical sciences Company Limited, Shekou, PR. China) was used for the estimation of troponin I levels.
Semi-automated auto-analyzer Microlab 300 (Vital scientific, Dieren, The Netherlands) was used for the measurement of enzymes activities: Total CK (TCK), CKMB isoenzymes, and LDH.
| Results|| |
Data obtained from the study are presented in the form of tables and figures. The results were analyzed using Microsoft Excel spreadsheet and statistical software Analyze-it for Microsoft Excel version 2.25 Excel 12 (The Tannery, 91 Kirkstall Road, Leeds, UK). P≤ 0.05 was considered statistically significant. One hundred and forty seropositive patients were included in the study, of which 89(63.6%) were females and 51(36.4%) were males. Forty-seven (33.6%) females (n = 89) were HIV-positive on antiretroviral drugs (HAART) and 42 (30%) were HIV-positive not on drugs. Twenty-three (16.4%) males (n = 51) were HIV-positive on antiretroviral drugs (HAART) while 28(20%) were HIV-positive not on drugs.
[Table 1] shows three groups in the study: HIV-positive patients on HAART, HIV-positive patients not yet on HAART, and HIV-negative controls. The mean concentrations of cTnI and serum biomarker (TCK, CKMB, and LDH) were significantly elevated in patients on HAART compared to HAART-naïve patients and controls, with the exception of TCK which was elevated in the HAART-naïve group compared to patients on HAART and controls; P values (<0.0001, 0.0265, 0.0007, and <0.0001) are statistically significant for cTnI, serum CKT (SCKT), serum CKMB (SCKMB), and serum LDH (SLDH), respectively. Serum levels of all parameters were decreasing with increasing duration of treatment, between the duration of <1–4 years but significantly increases between the duration of 5–6 years (P < 0.05) for all parameters with exception of LDH which show constant increase with increase in duration of treatments. The values were recorded in mean ± standard error of mean (SEM), as summarized in [Table 2].
|Table 1: Comparison of mean serum level of cardiac troponin I, total creatine kinase, creatine kinase muscle and brain subtype and lactate dehydrogenase levels (mean±standard mean of error) in patients and controls|
Click here to view
|Table 2: Effects of duration of highly active antiretroviral therapy treatment on serum cardiac troponin I, total creatine kinase, creatine kinase muscle and brain subtype and lactate dehydrogenase levels in highly active antiretroviral therapy group|
Click here to view
[Table 3] shows that of the 140 HIV-positive patients recruited for the present study, only 19 (13.6%) (mean ± SEM 0.23 ± 0.15; P = 0.15) patients have troponin I levels ≤0.5 ng/mL cutoff point. One hundred and twenty-one (86.4%) (mean ± SEM 3.65 ± 2.221; P= 0.0001) patients recorded the value between 0.56 and 149 ng/mL which were >0.5 ng/mL cutoff point. The highest value of troponin I recorded among the HIV-positive patients on HAART is 14.9 ng/mL, while a value of 8.5 ng/mL was recorded as the highest value among the HIV-positive patients not on HAART. Out of 121 (86.4%) with elevated cTnI, only 65 (53.7%) had elevated CKMB > 24 U/L. Of the one hundred and forty patients recruited in the study, 78 (55.7%) had elevated CKMB, of which 65 (83.3%) had elevated cTnI and all had elevated LDH.
|Table 3: Prevalence of cardiac troponin I and creatine kinase-muscle and brain elevation (mean±standard error of mean) among seropositive patients|
Click here to view
[Table 4] shows that the mean duration of HIV infection among studied subjects is mean ± SEM (2.25 ± 0.225) years (P < 0.0001). There was no significant correlation between the serum level of troponin I and other cardiac markers with (P = 0.7984, 0.1499, 0.0854, and 0.2144) for cTnI, SCKT, SCKMB, and SLDH, respectively (P > 0.05).
|Table 4: Correlation between duration of human immunodeficiency virus disease and serum levels of cardiac troponin I, total creatine kinase, creatine kinase muscle and brain subtype and lactate dehydrogenase in studied patients|
Click here to view
[Table 5] shows that the mean duration on HAART among the studied individuals is mean ± SEM (2.8 ± 0.29) years (P = 0.0001). There was no significant statistical correlation between the duration of drugs and serum level of cTnI and other cardiac enzymes (P = 0.1063, 0.2275, 0.1471, and 0.6856) for cTnI, SCKT, SCKMB and SLDH, respectively (P > 0.05).
|Table 5: Correlation between duration of highly active antiretroviral therapy and serum cardiac troponin I, total creatine kinase, creatine kinase muscle and brain subtype and lactate dehydrogenase levels (mean±standard error of mean) in patients on treatment|
Click here to view
[Table 6] shows that twenty seropositive patients on HAART were hypertensive (HPT) while fifty were non-HPT (NHPT). The HAART-naïve group and controls had only six HPT patients and 64 NHPT cases, respectively. cTnI level was not significantly elevated in treatment group (P > 0.05), but it was significantly elevated in HAART-naïve group with hypertension than in NHPT patients (P < 0.05). However, there was significant elevation of all the serum level these markers (cTnI, TCK, CKMB, and LDH) in patients than in controls.
|Table 6: Serum troponin I, total creatine kinase, creatine kinase muscle and brain subtype and lactate dehydrogenase levels (mean±standard error of mean) in hypertensive and nonhypertensive patients and controls|
Click here to view
[Table 7] shows that out of 140 patients, only 9 (6%) are smokers, 2 (1%) are females, and the remaining 8 (5%) are males. Among controls, 6 (9%) are smokers and are males. This indicates a significant correlation between serum level of cardiac enzymes but not in cTnI in the study group but statistically significant among controls and there is no direct association.
|Table 7: Correlation between duration of cigarette smoking and concentration of cardiac troponin I, total creatine kinase, creatine kinase muscle and brain subtype and lactate dehydrogenase among patients and controls|
Click here to view
| Discussion|| |
HIV and acquired immunodeficiency syndrome are problems affecting male and female, adult, and children worldwide.
The present study showed the cTnI concentration (mean ± SEM) in HIV-positive patients on drugs (HAART) and those not on drugs were significantly elevated (P < 0.05). For healthy controls, the cTnI value (mean ± SEM) remains low (P < 0.05). cTnI concentration (mean ± SEM) was reported to be elevated in hospitalized patients with heart failure, and also in healthy nonhospitalized control and hospitalized controls, respectively (P < 0.01 vs. heart failure patients). When both control groups were considered, the mean cTnI level was significantly elevated (P < 0.01 vs. heart failure patients), also reported that cTnI can be elevated in diseases other than acute coronary syndrome,, HIV inclusive. However, the serum cTnI does not increase to a much higher level. Their findings were corroborated with the present study which showed moderate elevation among HIV-positive patients on drugs and HIV-positive HAART-naïve patients, respectively, with highest value in this study of 14.9 ng/mL and lowest value was 0.01 ng/mL. One hundred and six patients (75.7%) had cTnI concentration above 1 ng/mL compared to 46 (65.7%) controls. In the control group, apart from one individual who had cTnI level of 11.56 ng/mL, the highest serum cTnI level was 5.68 ng/mL. This patient reported no history of cardiac event, diabetes mellitus, cigarette smoking or hypertension (BP 110/70 mmHg) which was thought to be due to lipid-lowering drug (statin) use reported by the subject. Furthermore, no individual reported history of chest pain in this study when compared to 3 cases out of 35 in another study, No history of MI was recorded in both patients and controls. In resource-limited areas like ours where facilities are mainly concerned with diagnoses and monitoring of patients with cardiovascular disease, cTnI assay can be used as an alternative considering its specificity and sensitivity by making it as routine test in emergency unit for risk stratification of patients for myocardial injury. Furthermore, the fact that cTnI persist for so long after MI suggest that finding above normal concentration of this marker could represent distant rather than very recent events. This corroborates our finding of elevated marker in clinically stable patients. Therefore, cTnI can be used for retrospective diagnosis of acute MI as reported by other study. If a biomarker is to be used to screen for uncommon condition in asymptomatic people, it should have high specificity because a rule in strategy is more important in this situation, this is the base for using cTnI as marker of subclinical cardiac injury in the current study, and it has a high specificity to cardiac muscles.
Similarly, serum CKMB was slightly elevated in both the HAART group and in non-HAART group but remained below the cutoff point in controls.
This finding was reported by another study, which shows that serum CKMB elevation in noncoronary syndromes group is less (6 ± 5 ng/mL) than in those with acute coronary syndromes (63 ± 54 ng/mL), a low CKMB value in a patient diagnosed as not having MI but with elevated cTnI level was reported. In this study, both groups had elevated CKMB. Out of 121 (86.4%) patients with elevated cTnI, only 65 (53.7%) had elevated CKMB level. The Joint Committee on redefinition of MI reported that measurement of total CK is not recommended for the routine diagnosis of acute MI because of the wide tissue distribution of this enzyme. Nevertheless, total CK has a long history, and some physicians may opt to continue to employ it for epidemiologic or scientific purposes. In such a setting, total CK should be combined with a more sensitive biomarker, such as cardiac troponin or CKMB, for more accurate clinical diagnosis of acute MI. This study has considered where we estimated cTnI and CKMB with total CK (mean ± SEM) among HIV-positive patients on HAART, HIV-positive patients not on HAART and controls, respectively, the values were less than the cutoff value for making diagnosis of MI. Statistically significant difference was reported in total creatine kinase (TCK) and CKMB between HIV-positive patients on HAART and those not on HAART, but not in LDH. In the present study, there were no statistically significant differences in TCK and CKMB (P = 0.347 and <0.069), respectively, but the difference in LDH was significant (P < 0.0036). HIV is known to affect cardiovascular system through various mechanisms., Metabolic abnormalities such as impaired glucose tolerance, hyperlipidemia, fat redistribution with central obesity, peripheral fat wasting and lactic acidosis are most widely studied secondary cardiovascular consequence of HIV infection, all of which increase the risk for artherosclerosis. Several studies,,, have shown that there was direct relation between HIV infection and cardiovascular disease.
The effect of HIV on vascular artherogenesis through monocytes-microphage infection via leukocytes adhesion, induction of inflammatory response in the endothelial lining of blood vessel and direct inversion of myocardium by virus and progressive tissue damage caused by virus was reported to induce chronic release of cytotoxic cytokines. The levels in biomarkers in the present study have shown no statistically significant relation with duration of the HIV disease, but the elevated level of the biomarker may also be as a result of the effect of virus itself on the cardiovascular system and not duration of the disease. Heart disease occurs late in the HIV infections, but in some cases, it occurs earlier and thus affecting prognosis of these patients. This may be the reason for elevated troponin I level among individuals in the present study with short history of 1 to 6 months duration since diagnosis 49 (35%). of these about 46 (93.9%) have cTnI concentration between (0.06 and 1.02 ng/mL) only 3 (6.1%) has cTnI concentration between (0.01 and 0.03 ng/mL). The results of clinical observation, results of clinical trials and the results of studies in healthy volunteers have documented metabolic effects on lipid metabolism by protease inhibitors (PIs), nucleoside reverse transcriptase inhibitors (NRTIs) and non-NRTIs (NNRTIs). PIs effect is related to an increase in hepatic very low-density lipoprotein secretion, NNRTIs effect may be related to an increase in the hepatic apo A 1 and capacity for lipoprotein secretion. In contrast, NRTIs seem to be indirect, it has been ascribed to mitochondrial toxicity., In the present study, all the recruited cases are taking NRTIs and NNRTIs containing regimen both of which have indirect effect on the heart muscle through altered lipid metabolism and mitochondrial toxicity, respectively. These are likely to explain the high elevation in cTnI concentration among HIV-seropositive patients on HAART than in HAART naïve, with mean concentration (3.323 ± 2.72 vs. 2.368 ± 1.84 ng/mL). There is no statistical correlation between HAART duration and serum level of cTnI, TCK, CKMB, and LDH. It was reported that HIV-infected patients receiving HAART have an increased risk of ischemic heart disease, but the relative risk is stable up to 8 years after treatment. This may explain the fluctuation of the biomarkers among the studied cases in our study.
However, history of traditional risk factors (diabetes mellitus, cigarette smoking, hypertension, and malnutrition) for cardiovascular diseases, especially MI, was also considered in the present study which showed no significant statistical relationship between the biomarker levels and these factors. There is statistically significant difference in systolic BP and diastolic BP among patients on HAART and those not yet on HAART. This is contrary to the findings in other researched works  that found no significant difference among two groups. Although none of the study cases had no clinical evidence of myocardial injury, the relatively low BP recorded among some of the patients may play a role in the cardiac event (90/60 mmHg) or high BP in some cases (180/100 mmHg). Some studies reported high prevalence of cigarette smoking among HIV-positive patients up to (22%), while its only 4.3% in the present study, this may not be unrelated to the culture and type of patients in the study (females).
| Conclusions|| |
This study found that for all parameters, HIV patients on HAART had statistically significant elevation of cTnI and other cardiac enzymes than in HIV HAART-naive patients. The study also demonstrated that cardiac injury is more likely to occur in HIV-positive patients on HAART when compared with HIV-positive HAART-naive patients as evident by biomarker level. The study also found that cTnI elevation were statistically significant in studied patients than in control, as such cTnI can be used for early detection of subclinical myocardial injury in HIV-positive patients. The variation in biomarker level seen between HIV-positive patients on HAART and HIV-positive naïve patients may not be unconnected to the toxicity of HAART drugs in patients on antiretroviral drugs.
We recommend further studies to determine the mechanism of cardiac injury in HIV patients since elevation of cTnI reflect myocardial damage but not the mechanism.
Longitudinal study is required to follow up the patients over the years for symptomatic cardiovascular disease.
Multidisciplinary collaboration may be useful for decision-making regarding the use of HAART and other drugs for monitoring and stratification of cardiovascular risk.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Sani MU, Okeahialam BN, Aliyu SH, Enoch DA. Human immunodeficiency virus (HIV) related heart disease: A review. Wien Klin Wochenschr 2005;117:73-81.
Bezante GP, Briatore L, Rollando D, Maggi D, Setti M, Ghio M, et al.
Hypoadiponectinemia in lipodystrophic HIV individuals; a metabolic marker of subclinical cardiac damage. Nutrition, Metabolism and cardiovascular Diseases 2009;19:277-82.
Hassan SI, editor. Essential Clinical Biochemistry. 1st
ed. Wusasa-Zaria, Nigeria: Tamaza Publishing Company Limited; 2007. p. 205-13.
Gilardi E, Paolo L, Davide M, Guido DM, Marcello C. Biomaker in the prediction and management of acute coronary syndromes: Current perspective. Res Rep Clin Cardiol 2014;5:21-31.
Missov E, Calzolari C, Pau B. Circulating cardiac troponin I in severe congestive heart failure. Circulation 1997;96:2953-8.
Katus HA, Remppis A, Neumann FJ, Scheffold T, Diederich KW, Vinar G, et al.
Diagnostic efficiency of troponin T measurements in acute myocardial infarction. Circulation 1991;83:902-12.
Adams JE 3rd
, Bodor GS, Dávila-Román VG, Delmez JA, Apple FS, Ladenson JH, et al.
Cardiac troponin I. A marker with high specificity for cardiac injury. Circulation 1993;88:101-6.
Jaffe AS, Landt Y, Parvin CA, Abendschein DR, Geltman EM, Ladenson JH. Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction. Clin Chem 1996;42:1770-6.
Jaffe AS, Ravkilde J, Roberts R, Naslund U, Apple FS, Galvani M, et al.
It's time for a change to a troponin standard. Circulation 2000;102:1216-20.
Ijaz AK, Aung T, Norrapol W, Moe TW, Tin AH, Akhtar H, et al
. Elevation of serum cardiac troponin I in non cardiac and cardiac diseases other than acute coronary syndromes. Am J Emerg Med 1999;17:225-9.
European Society of Cardiology/American College of Cardiology ESC/ACC. Myocardial infarction redefined. J Am Coll Cardiol 2000;36:1502-13.
Araoye MO, editor. Research methodology with statistic for health and social sciences. Ilorin, Nigeria: NA THERDEX Publishers; 2003. p. 115-29.
Tanindi A, Cemri M. Troponin elevation in conditions other than acute coronary syndromes. Vasc Health Risk Manag 2011;7:597-603.
Vasan RS. Biomarkers of cardiovascular disease: Molecular basis and practical considerations. Circulation 2006;113:2335-62.
Adams JE 3rd
, Schechtman KB, Landt Y, Ladenson JH, Jaffe AS. Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I. Clin Chem 1994;40(7 Pt 1):1291-5.
Oluboyo AO, Okogun GR, DURU LAD, Oluboyo BO, Emenike F, et al
. Pattern of blood pressure, CD4+ T cells counts and some cardiac enzymes in HIV seropositive subjects. J Biomed Invest 2006;4:32-41.
Currier SJ. Update on cardiovascular complications in HIV infection a perspective. Int AIDS Soc USA 2009;17:98-103.
Dubé MP, Lipshultz SE, Fichtenbaum CJ, Greenberg R, Schecter AD, Fisher SD; Working Group. Effects of HIV infection and antiretroviral therapy on the heart and vasculature. Circulation 2008;118:e36-40.
Panther LA. How HIV infection and its treatment affects the cardiovascular system: What is known, what is needed. Am J Physiol Heart Circ Physiol 2002;283:H1-4.
Barbaro G, Barbarini G. Human immunodeficiency virus & cardiovascular risk. Indian J Med Res 2011;134:898-903.
] [Full text]
Barbaro G. Cardiovascular manifestations of HIV infection. Circulation 2002;106:1420-5.
Sani MU. Myocardial disease in human immunodeficiency virus (HIV) infection: A review. Wien Klin Wochenschr 2008;120:77-87.
Sánchez-Torres RJ, García-Palmieri MR. Cardiovascular disease in HIV infection.P R Health Sci J 2006;25:249-54.
Kotler DP. HIV and antiretroviral therapy: Lipid abnormalities and associated cardiovascular risk in HIV-infected patients. J Acquir Immune Defic Syndr 2008;49 Suppl 2:S79-85.
Liang JS, Distler O, Cooper DA, Jamil H, Deckelbaum RJ, Ginsberg HN, et al.
HIV protease inhibitors protect apolipoprotein B from degradation by the proteasome: A potential mechanism for protease inhibitor-induced hyperlipidemia. Nat Med 2001;7:1327-31.
Obel N, Thomsen HF, Kronborg G, Larsen CS, Hildebrandt PR, SÂrensen HT, et al.
Ischemic heart disease in HIV-infected and HIV-uninfected individuals: A population-based cohort study. Clin Infect Dis 2007;44:1625-31.
Triant VA, Lee H, Hadigan C, Grinspoon SK. Increased acute myocardial infarction rates and cardiovascular risk factors among patients with human immunodeficiency virus disease. J Clin Endocrinol Metab 2007;92:2506-12.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]