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Human immunodeficiency virus-infected subjects have no altered myocardial perfusion
International Journal of Cardiology 122 (2007) 90 – 92 www.elsevier.com/locate/ijcard
Letter to the Editor
Human immunodeficiency virus-infected subjects have no altered myocardial perfusion ☆ Andres Catzin-Kuhlmann a , Arturo Orea-Tejeda b , Lilia Castillo-Martínez b , Eloisa Colín-Ramírez b , Daniel Asz c , Víctor H. Aguirre c , Luis E. Herrera c , Victoria Valles d , Carlos A. Aguilar-Salinas d , Juan Sierra e , Juan J. Calva c,⁎ Department of Medicine, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico Division of Cardiology, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico c Clinical Epidemiology Unit, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico Division of Endocrinology and Metabolism, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico e Division of Infectious Diseases, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico a
b
d
Received 17 August 2006; accepted 2 November 2006 Available online 26 January 2007
Abstract We assessed myocardial perfusion (blinded interpretation of a single-photon emission computed tomography) and known risk factors for atherosclerosis in 105 randomly selected human immunodeficiency virus (HIV)-infected patients in a clinic in Mexico City and in a community sample of 105 age and gender-matched infection-free subjects. An abnormal scan was obtained in 4.8% of the infected and in 7.6% of the non-infected subjects. Severity of scintigraphic abnormalities was similar in both groups. In these Mexican HIV-infected patients, despite a long time of infection and of exposure to combined antiretroviral therapy and to other classical risk factors for atherosclerosis, there was no evidence of increased risk for abnormal myocardial perfusion. Dissimilar magnitude in the hazard of coronary heart disease may occur among infected populations with different frequencies of traditional predisposing factors for cardiovascular illness. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Human immunodeficiency virus; Coronary disease; Tomography; Emission-computed; Single-photon; Antiretroviral therapy
After several years of human immunodeficiency virus (HIV) infection and of antiretroviral therapy (ART) exposure, patients could be at increased risk of premature coronary heart disease (CHD); yet there is still no consistent and methodologically sound evidence to support this hypothesis. Previous epidemiologic studies addressing it show conflicting results [1–8] or flawed conclusions due to biases. It is relevant to assess the functional translation (myocardial
☆ Grant support: Mexico's National Council of Science and Technology (CONACYT) grant 2002-C01–42074. ⁎ Corresponding author. Clinical Epidemiology Unit, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Vasco de Quiroga 15, Sección XVI, Tlalpan, 14000 México, D.F., Mexico. Tel.: +52 55 55730727; fax: +52 55 56557404. E-mail address: [email protected] (J.J. Calva).
0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.11.040
perfusion) of the structural changes (such as coronary calcium) [7] documented in HIV-infected individuals, no research regarding this has been published. This study was designed to test the hypothesis that HIV-infected patients were more likely to have abnormal myocardial perfusion, as measured by single-photon emission computed tomography (SPECT), than age and gender-matched HIVfree individuals. In a cross-sectional survey with sampling by exposure 105 patients were randomly selected from the 513 regular attendants of Mexico's National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’ (a tertiary care adult referral center) HIV clinic and constituted the HIV-infected (exposed) sample. Age and gender-matched relatives, neighbors, or friends of these patients negative for serum HIV antibodies by the enzyme-linked immunosorbent assay became the HIV-
A. Catzin-Kuhlmann et al. / International Journal of Cardiology 122 (2007) 90–92
non-infected (non-exposed community volunteers) comparison group (n = 105). Each one of the 210 participants signed an informed consent form, which, along with the study protocol, was previously approved by the Institute's ethics committee. From July 2003 to February 2004 exactly the same data from all participants were prospectively obtained. After an overnight fast, peripheral venous blood was drawn and tested for triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, apolipoprotein A-I, apolipoprotein B, lipoprotein (a), glucose, insulin, fibrinogen, homocysteine, and high sensitivity C-reactive protein (hsCRP). Subjects underwent a standardized anthropometric evaluation (including bioelectric impedance) by trained personnel. Through a face-to-face interview a structured questionnaire was applied, which assessed demographic, lifestyle, and co-morbidity issues. Personal as well as family history (before the age of 60) of vascular disease (myocardial infarction, stroke, angina), drug abuse, present and past active tobacco smoke inhalation, physical activity, diet quality, alcohol consumption; and presence, time since diagnosis, and current treatment of diabetes mellitus and arterial hypertension were interrogated. After measurement of their resting blood pressure by the auscultatory method all subjects underwent a gated SPECT with technetium-99 sestamibi (one-day rest–stress imaging protocol), according to the guidelines of the American Society of Nuclear Cardiology [9]. The images were interpreted by a nuclear cardiology expert blinded to the HIV infection status of the subjects. Information about the HIV-infected patients, such as time since diagnosis of infection, CD4-positive cell counts, plasma virus loads, and type and duration of ART, was retrieved from hospital records. None of the 210 participants had a personal history of unstable angina or myocardial infarction, nor did any one have left bundle branch block. None of the subjects with abnormal SPECT reported having had angina-like chest pain. The 105 HIV-positive patients had a median time since infection diagnosis of 55.8 months [interquartile range (IQR) = 32.6– 80.3]. Ninety-seven (92%) were receiving combined ART and had taken it during a median time of 41.8 months (IQR = 22.4– 71.6); the remaining 8 patients were treatment-naïve. All patients under therapy had been exposed to nucleoside reverse transcriptase inhibitors (median time in all 105 of 38.7 months; IQR = 19.3–69.3), 70 (67%) to protease inhibitors (median time in all 105 of 18.7 months; IQR = 0–48.8), and 68 (65%) to non-nucleoside reverse transcriptase inhibitors (median time in all 105 of 9.3 months; IQR = 0–24). Median nadir CD4positive lymphocyte count was 146 cells/mm3 (IQR = 63– 261); and the proportion of patients with undetectable plasma viral load (at least 2 consecutive loads of less than 50 copies/ ml), with detectable plasma HIV ribonucleic acid after having reached undetectable levels, and with no documentation of at least 2 consecutive undetectable plasma levels at any time, was 73%, 6%, and 21%, respectively. In contrast to infected patients, infection-free individuals had larger body-fat percentage, body mass index, and waist circumference; and a greater rate of hypertension. Conversely, HIV-positive patients
91
had lower scores of physical activity and of alcohol consumption, a smaller limb/trunk skin folds ratio (thus more centripetal fat accumulation), higher median triglycerides, lower median HDL cholesterol, and higher median hsCRP, compared to non-infected subjects. The frequencies of the remaining measured risk factors for CHD were similar in both groups (Table 1). Subjects with an abnormal SPECT had a Table 1 Comparison of human immunodeficiency virus-infected with non-infected subjects Feature
Male gender Age (years) Family history of early vascular disease Current smoking Physical activity (index) Diet (index) Alcohol (b3 drinks/week) Triglycerides (mg/dL) Total cholesterol (mg/dL) High density lipoprotein cholesterol (mg/dL) Apolipoprotein A-I (mg/dL) Apolipoprotein B (mg/dL) Lipoprotein (a) (mg/dL) Diabetes mellitus Impaired fasting glucose Insulin (μU/mL) Homeostasis Model Assessment ⁎ Fibrinogen (case/control) Homocysteine (μmol/L) High sensitivity C-reactive protein (mg/L) Body-fat (%) Body mass index (kg/m2) Waist circumference (cm) Skin folds ratio (limb/trunk) Arterial hypertension Metabolic syndrome 10-year coronary heart disease risk (Framingham scoring) (%) 10-year coronary heart disease risk b 10% 10-year coronary heart disease risk 10–20% 10-year coronary heart disease risk N 20%
Human immunodeficiency virus-negative (n = 105)
Human P immunodeficiency value virus-positive (n = 105)
85 (81%) 38 (31–47) 15 (14%)
85 (81%) 37 (32–44) 22 (21%)
ns ns ns
45 (43%) 24 (13–31) 77 (70–84) 85 (81%)
34 (32%) 17 (10–27) 77 (70–84) 98 (93%)
ns 0.03 ns 0.007
155 (99–255) 186 (163–219) 36 (32–42)
230 (156–345) 173 (148–210) 33 (29–40)
98 (88–106)
93 (86–105)
ns
100 (88–118)
98 (81–116)
ns
6.7 (3.3–20.1) 9 (9%) 18 (17%) 10.6 (7.3–16.7) 2.56 (1.68–3.93)
7.3 (3.5–15) 11 (11%) 11 (11%) 10.2 (6.8–16.4) 2.44 (1.57–3.77)
ns ns ns ns ns
1.16 (0.97–1.35) 11.1 (9.2–13.4) 1.72 (0.88–4.3)
1.09 (0.88–1.47) 10.7 (8.2–13.1) 2.36 (1–6.29)
ns ns 0.03
28 (24–31) 28.8 (26.3–32) 94 (88–100)
24 (20–27) 25.5 (23–27.9) 87 (82–91)
b0.001 b0.001 b0.001
0.73 (0.56–0.87)
0.59 (0.48–0.73)
b0.001
b0.001 ns 0.02
33 (31%) 36 (34%) 2 (1–6)
18 (17%) 25 (24%) 1 (1–3)
0.02 ns ns
85 (81%)
92 (88%)
ns
17 (16%)
13 (12%)
ns
3 (2.9%)
0
ns
Data are presented as number of patients (percentage) or median (interquartile range). ns = not significant. ⁎ [glucose (mmol/L) × insulin (μU/mL)] / 22.5.
92
A. Catzin-Kuhlmann et al. / International Journal of Cardiology 122 (2007) 90–92
Table 2 Comparison of altered image type between infected and non-infected subjects with abnormal single-photon emission computed tomography Vessels (#)
Reverse reversibility [territories (severity)]
Ischemia [territories (severity)]
Human immunodeficiency virus-negative (n = 8) 2 8 (2) 4 2 3 (3) 3 2 17 (3) 0 1 0 6 1 0 4 1 2 (3) 0 1 2 (2) 0 1 2 (2) 0
(1) (3) (3) (2)
Human immunodeficiency virus-positive (n = 5) 2 17 (1) 0 1 4 (2) 4 (3) 1 0 4 (2) 1 5 (2) 0 1 3 (2) 0
Necrosis [territories (severity)] 0 0 0 4 (2) 0 0 0 0
abnormal myocardial perfusion in Mexican highly active ART-treated, HIV-infected patients with a high prevalence of hypertriglyceridemia and low HDL cholesterol as well as of circulating markers of inflammation. The hypothesis of a causal relationship between HIV infection or its therapy and early CHD has still no sound and consistent support, and other risk determinants of CHD may play a major role. Our finding supports the concept of a much more complex interaction between the virus, ART and classical risk factors as potential determinants of premature CHD. Dissimilar hazard magnitude of CHD may occur in diverse HIVpositive populations with different frequencies of traditional predisposing factors for cardiovascular illness. References
0 0 0 0 0
larger median waist circumference (95 versus 90 cm; p = 0.03) and a higher median 10-year CHD risk by Framingham scoring (4 versus 2%; p = 0.04). We detected a prevalence of 4.8% [95% confidence interval (CI) = 1.5–10.8] of abnormal myocardial perfusion in HIV-infected patients versus 7.6% (95% CI = 3.3–14.5) in non-infected subjects. No evidence of an increased likelihood of abnormal myocardial perfusion in infected patients was found as both crude and potential confounders (waist circumference and 10-year CHD risk by Framingham scoring)-adjusted odds ratios (OR) were not different from unit (adjusted OR = 0.54; 95% CI = 0.13–2.25). The number of affected coronary vessels and of myocardial territories showing ischemia and/or necrosis was not significantly different between both groups (Table 2). There is no publication about myocardial perfusion in HIV infection. Our epidemiological study was designed to minimize potential sampling and susceptibility biases and to have enough statistical power to detect a clinically important difference. We found no evidence of an increased risk for
[1] Barbaro G, Di Lorenzo G, Cirelli A, et al. An open-label, prospective, observational study of the incidence of coronary artery disease in patients with HIV infection receiving highly active antiretroviral therapy. Clin Ther 2003;25:2405–18. [2] Bozzette SA, Ake CF, Tam HK, Chang SW, Louis TA. Cardiovascular and cerebrovascular events in patients treated for human immunodeficiency virus infection. N Engl J Med 2003;348:702–10. [3] Currier JS, Taylor A, Boyd F, et al. Coronary heart disease in HIVinfected individuals. J Acquir Immune Defic Syndr 2003;33:506–12. [4] Holmberg SD, Moorman AC, Williamson JM, et al. Protease inhibitors and cardiovascular outcomes in patients with HIV-1. Lancet 2002;360:1747–8. [5] Klein D, Hurley LB, Quesenberry CP, Sidney S. Do protease inhibitors increase the risk for coronary heart disease in patients with HIV-1 infection? J Acquir Immune Defic Syndr 2002;30:471–7. [6] Mary-Krause M, Cotte L, Simon A, Partisani M, Costogliola D, and the Clinical Epidemiology Group from the French Hospital Database. Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men. AIDS 2003;17:2479–86. [7] Talwani R, Falusi OM, Mendes de Leon CF, et al. Electron beam computed tomography for assessment of coronary artery disease in HIVinfected men receiving antiretroviral therapy. J Acquir Immune Defic Syndr 2002;30:191–5. [8] The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) Study Group. Combination antiretroviral therapy and the risk of myocardial infarction. N Engl J Med 2003;349:1993–2003. [9] American Society of Nuclear Cardiology. Updated imaging guidelines for nuclear cardiology procedures, part 1. J Nucl Cardiol Jan–Feb 2001;8(1): G5–G58.
Letter to the Editor
Human immunodeficiency virus-infected subjects have no altered myocardial perfusion ☆ Andres Catzin-Kuhlmann a , Arturo Orea-Tejeda b , Lilia Castillo-Martínez b , Eloisa Colín-Ramírez b , Daniel Asz c , Víctor H. Aguirre c , Luis E. Herrera c , Victoria Valles d , Carlos A. Aguilar-Salinas d , Juan Sierra e , Juan J. Calva c,⁎ Department of Medicine, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico Division of Cardiology, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico c Clinical Epidemiology Unit, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico Division of Endocrinology and Metabolism, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico e Division of Infectious Diseases, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Mexico a
b
d
Received 17 August 2006; accepted 2 November 2006 Available online 26 January 2007
Abstract We assessed myocardial perfusion (blinded interpretation of a single-photon emission computed tomography) and known risk factors for atherosclerosis in 105 randomly selected human immunodeficiency virus (HIV)-infected patients in a clinic in Mexico City and in a community sample of 105 age and gender-matched infection-free subjects. An abnormal scan was obtained in 4.8% of the infected and in 7.6% of the non-infected subjects. Severity of scintigraphic abnormalities was similar in both groups. In these Mexican HIV-infected patients, despite a long time of infection and of exposure to combined antiretroviral therapy and to other classical risk factors for atherosclerosis, there was no evidence of increased risk for abnormal myocardial perfusion. Dissimilar magnitude in the hazard of coronary heart disease may occur among infected populations with different frequencies of traditional predisposing factors for cardiovascular illness. © 2006 Elsevier Ireland Ltd. All rights reserved. Keywords: Human immunodeficiency virus; Coronary disease; Tomography; Emission-computed; Single-photon; Antiretroviral therapy
After several years of human immunodeficiency virus (HIV) infection and of antiretroviral therapy (ART) exposure, patients could be at increased risk of premature coronary heart disease (CHD); yet there is still no consistent and methodologically sound evidence to support this hypothesis. Previous epidemiologic studies addressing it show conflicting results [1–8] or flawed conclusions due to biases. It is relevant to assess the functional translation (myocardial
☆ Grant support: Mexico's National Council of Science and Technology (CONACYT) grant 2002-C01–42074. ⁎ Corresponding author. Clinical Epidemiology Unit, National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’, Vasco de Quiroga 15, Sección XVI, Tlalpan, 14000 México, D.F., Mexico. Tel.: +52 55 55730727; fax: +52 55 56557404. E-mail address: [email protected] (J.J. Calva).
0167-5273/$ - see front matter © 2006 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2006.11.040
perfusion) of the structural changes (such as coronary calcium) [7] documented in HIV-infected individuals, no research regarding this has been published. This study was designed to test the hypothesis that HIV-infected patients were more likely to have abnormal myocardial perfusion, as measured by single-photon emission computed tomography (SPECT), than age and gender-matched HIVfree individuals. In a cross-sectional survey with sampling by exposure 105 patients were randomly selected from the 513 regular attendants of Mexico's National Institute of Medical Sciences and Nutrition ‘Salvador Zubirán’ (a tertiary care adult referral center) HIV clinic and constituted the HIV-infected (exposed) sample. Age and gender-matched relatives, neighbors, or friends of these patients negative for serum HIV antibodies by the enzyme-linked immunosorbent assay became the HIV-
A. Catzin-Kuhlmann et al. / International Journal of Cardiology 122 (2007) 90–92
non-infected (non-exposed community volunteers) comparison group (n = 105). Each one of the 210 participants signed an informed consent form, which, along with the study protocol, was previously approved by the Institute's ethics committee. From July 2003 to February 2004 exactly the same data from all participants were prospectively obtained. After an overnight fast, peripheral venous blood was drawn and tested for triglycerides, total cholesterol, high density lipoprotein (HDL) cholesterol, apolipoprotein A-I, apolipoprotein B, lipoprotein (a), glucose, insulin, fibrinogen, homocysteine, and high sensitivity C-reactive protein (hsCRP). Subjects underwent a standardized anthropometric evaluation (including bioelectric impedance) by trained personnel. Through a face-to-face interview a structured questionnaire was applied, which assessed demographic, lifestyle, and co-morbidity issues. Personal as well as family history (before the age of 60) of vascular disease (myocardial infarction, stroke, angina), drug abuse, present and past active tobacco smoke inhalation, physical activity, diet quality, alcohol consumption; and presence, time since diagnosis, and current treatment of diabetes mellitus and arterial hypertension were interrogated. After measurement of their resting blood pressure by the auscultatory method all subjects underwent a gated SPECT with technetium-99 sestamibi (one-day rest–stress imaging protocol), according to the guidelines of the American Society of Nuclear Cardiology [9]. The images were interpreted by a nuclear cardiology expert blinded to the HIV infection status of the subjects. Information about the HIV-infected patients, such as time since diagnosis of infection, CD4-positive cell counts, plasma virus loads, and type and duration of ART, was retrieved from hospital records. None of the 210 participants had a personal history of unstable angina or myocardial infarction, nor did any one have left bundle branch block. None of the subjects with abnormal SPECT reported having had angina-like chest pain. The 105 HIV-positive patients had a median time since infection diagnosis of 55.8 months [interquartile range (IQR) = 32.6– 80.3]. Ninety-seven (92%) were receiving combined ART and had taken it during a median time of 41.8 months (IQR = 22.4– 71.6); the remaining 8 patients were treatment-naïve. All patients under therapy had been exposed to nucleoside reverse transcriptase inhibitors (median time in all 105 of 38.7 months; IQR = 19.3–69.3), 70 (67%) to protease inhibitors (median time in all 105 of 18.7 months; IQR = 0–48.8), and 68 (65%) to non-nucleoside reverse transcriptase inhibitors (median time in all 105 of 9.3 months; IQR = 0–24). Median nadir CD4positive lymphocyte count was 146 cells/mm3 (IQR = 63– 261); and the proportion of patients with undetectable plasma viral load (at least 2 consecutive loads of less than 50 copies/ ml), with detectable plasma HIV ribonucleic acid after having reached undetectable levels, and with no documentation of at least 2 consecutive undetectable plasma levels at any time, was 73%, 6%, and 21%, respectively. In contrast to infected patients, infection-free individuals had larger body-fat percentage, body mass index, and waist circumference; and a greater rate of hypertension. Conversely, HIV-positive patients
91
had lower scores of physical activity and of alcohol consumption, a smaller limb/trunk skin folds ratio (thus more centripetal fat accumulation), higher median triglycerides, lower median HDL cholesterol, and higher median hsCRP, compared to non-infected subjects. The frequencies of the remaining measured risk factors for CHD were similar in both groups (Table 1). Subjects with an abnormal SPECT had a Table 1 Comparison of human immunodeficiency virus-infected with non-infected subjects Feature
Male gender Age (years) Family history of early vascular disease Current smoking Physical activity (index) Diet (index) Alcohol (b3 drinks/week) Triglycerides (mg/dL) Total cholesterol (mg/dL) High density lipoprotein cholesterol (mg/dL) Apolipoprotein A-I (mg/dL) Apolipoprotein B (mg/dL) Lipoprotein (a) (mg/dL) Diabetes mellitus Impaired fasting glucose Insulin (μU/mL) Homeostasis Model Assessment ⁎ Fibrinogen (case/control) Homocysteine (μmol/L) High sensitivity C-reactive protein (mg/L) Body-fat (%) Body mass index (kg/m2) Waist circumference (cm) Skin folds ratio (limb/trunk) Arterial hypertension Metabolic syndrome 10-year coronary heart disease risk (Framingham scoring) (%) 10-year coronary heart disease risk b 10% 10-year coronary heart disease risk 10–20% 10-year coronary heart disease risk N 20%
Human immunodeficiency virus-negative (n = 105)
Human P immunodeficiency value virus-positive (n = 105)
85 (81%) 38 (31–47) 15 (14%)
85 (81%) 37 (32–44) 22 (21%)
ns ns ns
45 (43%) 24 (13–31) 77 (70–84) 85 (81%)
34 (32%) 17 (10–27) 77 (70–84) 98 (93%)
ns 0.03 ns 0.007
155 (99–255) 186 (163–219) 36 (32–42)
230 (156–345) 173 (148–210) 33 (29–40)
98 (88–106)
93 (86–105)
ns
100 (88–118)
98 (81–116)
ns
6.7 (3.3–20.1) 9 (9%) 18 (17%) 10.6 (7.3–16.7) 2.56 (1.68–3.93)
7.3 (3.5–15) 11 (11%) 11 (11%) 10.2 (6.8–16.4) 2.44 (1.57–3.77)
ns ns ns ns ns
1.16 (0.97–1.35) 11.1 (9.2–13.4) 1.72 (0.88–4.3)
1.09 (0.88–1.47) 10.7 (8.2–13.1) 2.36 (1–6.29)
ns ns 0.03
28 (24–31) 28.8 (26.3–32) 94 (88–100)
24 (20–27) 25.5 (23–27.9) 87 (82–91)
b0.001 b0.001 b0.001
0.73 (0.56–0.87)
0.59 (0.48–0.73)
b0.001
b0.001 ns 0.02
33 (31%) 36 (34%) 2 (1–6)
18 (17%) 25 (24%) 1 (1–3)
0.02 ns ns
85 (81%)
92 (88%)
ns
17 (16%)
13 (12%)
ns
3 (2.9%)
0
ns
Data are presented as number of patients (percentage) or median (interquartile range). ns = not significant. ⁎ [glucose (mmol/L) × insulin (μU/mL)] / 22.5.
92
A. Catzin-Kuhlmann et al. / International Journal of Cardiology 122 (2007) 90–92
Table 2 Comparison of altered image type between infected and non-infected subjects with abnormal single-photon emission computed tomography Vessels (#)
Reverse reversibility [territories (severity)]
Ischemia [territories (severity)]
Human immunodeficiency virus-negative (n = 8) 2 8 (2) 4 2 3 (3) 3 2 17 (3) 0 1 0 6 1 0 4 1 2 (3) 0 1 2 (2) 0 1 2 (2) 0
(1) (3) (3) (2)
Human immunodeficiency virus-positive (n = 5) 2 17 (1) 0 1 4 (2) 4 (3) 1 0 4 (2) 1 5 (2) 0 1 3 (2) 0
Necrosis [territories (severity)] 0 0 0 4 (2) 0 0 0 0
abnormal myocardial perfusion in Mexican highly active ART-treated, HIV-infected patients with a high prevalence of hypertriglyceridemia and low HDL cholesterol as well as of circulating markers of inflammation. The hypothesis of a causal relationship between HIV infection or its therapy and early CHD has still no sound and consistent support, and other risk determinants of CHD may play a major role. Our finding supports the concept of a much more complex interaction between the virus, ART and classical risk factors as potential determinants of premature CHD. Dissimilar hazard magnitude of CHD may occur in diverse HIVpositive populations with different frequencies of traditional predisposing factors for cardiovascular illness. References
0 0 0 0 0
larger median waist circumference (95 versus 90 cm; p = 0.03) and a higher median 10-year CHD risk by Framingham scoring (4 versus 2%; p = 0.04). We detected a prevalence of 4.8% [95% confidence interval (CI) = 1.5–10.8] of abnormal myocardial perfusion in HIV-infected patients versus 7.6% (95% CI = 3.3–14.5) in non-infected subjects. No evidence of an increased likelihood of abnormal myocardial perfusion in infected patients was found as both crude and potential confounders (waist circumference and 10-year CHD risk by Framingham scoring)-adjusted odds ratios (OR) were not different from unit (adjusted OR = 0.54; 95% CI = 0.13–2.25). The number of affected coronary vessels and of myocardial territories showing ischemia and/or necrosis was not significantly different between both groups (Table 2). There is no publication about myocardial perfusion in HIV infection. Our epidemiological study was designed to minimize potential sampling and susceptibility biases and to have enough statistical power to detect a clinically important difference. We found no evidence of an increased risk for
[1] Barbaro G, Di Lorenzo G, Cirelli A, et al. An open-label, prospective, observational study of the incidence of coronary artery disease in patients with HIV infection receiving highly active antiretroviral therapy. Clin Ther 2003;25:2405–18. [2] Bozzette SA, Ake CF, Tam HK, Chang SW, Louis TA. Cardiovascular and cerebrovascular events in patients treated for human immunodeficiency virus infection. N Engl J Med 2003;348:702–10. [3] Currier JS, Taylor A, Boyd F, et al. Coronary heart disease in HIVinfected individuals. J Acquir Immune Defic Syndr 2003;33:506–12. [4] Holmberg SD, Moorman AC, Williamson JM, et al. Protease inhibitors and cardiovascular outcomes in patients with HIV-1. Lancet 2002;360:1747–8. [5] Klein D, Hurley LB, Quesenberry CP, Sidney S. Do protease inhibitors increase the risk for coronary heart disease in patients with HIV-1 infection? J Acquir Immune Defic Syndr 2002;30:471–7. [6] Mary-Krause M, Cotte L, Simon A, Partisani M, Costogliola D, and the Clinical Epidemiology Group from the French Hospital Database. Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men. AIDS 2003;17:2479–86. [7] Talwani R, Falusi OM, Mendes de Leon CF, et al. Electron beam computed tomography for assessment of coronary artery disease in HIVinfected men receiving antiretroviral therapy. J Acquir Immune Defic Syndr 2002;30:191–5. [8] The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) Study Group. Combination antiretroviral therapy and the risk of myocardial infarction. N Engl J Med 2003;349:1993–2003. [9] American Society of Nuclear Cardiology. Updated imaging guidelines for nuclear cardiology procedures, part 1. J Nucl Cardiol Jan–Feb 2001;8(1): G5–G58.