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Indian Journal for the Practising Doctor

Does HIV Infection Afford a Prevention from Hypertension?

Author(s): Rampal V, Ahmad M

Vol. 5, No. 6 (2009-01 - 2009-02)

Rampal V, Ahmad M

Dr Vinay Rampal, Physician Specialist, Government Medical College, Jammu
Dr Muzzafar Ahmad, Director Health Services, Kashmir (Jandamp;K)

ISSN: 0973-516X

Introduction

HIV infection, a global pandemic is engulfing the world like plague. However, there are some fields where this immunocompromised state might bring some respite to sufferers of chronic diseases like Rheumatoid Arthritis. Although HIV has no definitive cure, still HAART may give more years of comfortable living with longevity. This longevity may further be associated with development of age-related disorders like Hypertension, Diabetes mellitus, CHOAD and IHD, more so because HAART may induce dyslipidemia, insulin resistance and a body fat distribution similar to that seen in the Metabolic syndrome. Hypertension is often a part of this classic metabolic syndrome. HIV infection itself might afflict the kidneys in the form of HIV-associated nephropathy (HIVAN), thus enhancing hypertension-related kidney dysfunction. Besides affecting the choice of antihypertensives, in the light of drug interactions between various HAART regimes and antihypertensives (NNRTIs v/s CCBs and PIs v/s BBs), concomitant presence of the two diseases, also poses a challenge to the treating physician. In the western literature, the treatment of hypertension has been advocated the same as in chronic kidney disease and diabetes mellitus, because of the impending HIVAN. Some studies have also reported a reduced incidence of hypertension in the HIV- infected population as compared to the non-HIV infected population and the HIV-infected populace on HAART.

Paradoxical though, but we are presenting a study wherein HIV infection seems to act as a shield to the onset of hypertension in individuals with a positive family history of hypertension. No such study has been reported so far from our subcontinent.

Methods

Thirty patients, all males, aged 34-55 years (belonging to a particular community and uprooted from the place of their origin) with a positive family history of hypertension and the prevalence of HCVD in their siblings who on routine testing for blood donation turned out to be HIV+ were followed-up for a period of 15 months from April 2007 to June 2008. These persons were not hypertensive at the detection and their basal parameters including lipid profile, chest xray, ECG funduscopy, USG abdomen and Echocardiography (where needed) were carried out and repeated every 3 months. They were compared to their siblings (18 cases ) and other matched (age, sex and BMI) controls from their community (12 cases), since they were confined to certain hamlets having similar living conditions, the same supply of ration, similar pattern of clothing, similar occupation as well as per capita income and other habits besides being exposed to similar emotional circumstances.

Observations/Results

Out of 30 patients, only 6 developed hypertension at a mean age of 42 years, (age of onset being respectively 37, 38, 40, 42, 45 and 50 years). The first (pt no.1) to develop hypertension was a 40year old bachelor, a chronic smoker as well as an alcoholic whose blood pressure readings started showing a swing towards higher side by the 6th week of follow–up. When the advice to stop alcohol and smoking besides ‘Dietary Approaches to Stop Hypertension’ (DASH) did not yield a positive result, he had to be put on anti-hypertensives (a combination of an ARB + thiazide diuretic) by the 12th week. The second one (pt no. 2) to manifest hypertension was a 50 year old married teacher, also a chronic smoker but an occasional drinker, who presented with pedal edema in the 10th week needing a thiazide diuretic with addition of an ARB lateron. The other four (pts No. 3, 4, 5 and 6) aged 45,42,38 and 37 (all married) manifested signs of hypertension by 14th to 20th week of follow-up needing 2.5to 5mg of an ACE-inhibitor. Three out of these 6 (pt no 1, 2 and 3) needing antihypertensive drugs, showed left atrial enlargement and early left ventricular hypertrophy and funduscopic changes, grade 1 and 2. Patient no.1 also showed mild proteinuria besides altered renal parameters without any alteration in the echographic changes in the kidneys or heart. With continuous therapy, control over smoking and alcohol and DASH, there was a favourable response in all the six hypertensives and after winter (when there was slight worsening) the blood pressure levels showed a gradual fall and the doses of drugs were tapered off, and by the 12th month only 2 patients were receiving anti-hypertensives, and by the end of 15th month there was only one patient on therapy. The remaining 24, showing a variation in the blood pressure levels now and then, never needed any pharmacological intervention nor did their parameters i.e. Chest xray, ECG or funduscopy show any signs of hypertensive changes. All the 30 patients showed a rise in cholesterol, triglycerides and LDL levels in the beginning irrespective of their hypertensive status or CD4+T cell count with a nadir at the 24th week, however, with a return to normal by the 12th month without any pharmacotherapy.

The controls, on the other hand, developed hypertension along with its attendant stigmata, starting right from the 8th week of follow-up ( in those above 45years) to the 18th week in the youngest, with a climax at the 32nd week when all of them had to be put on a combination of anti-hypertensives (a BB + a diuretic or an ACEI+CCB). Fifteen of them developed ECG changes and 10 developed funduscopic changes with alterations in renal functions. Four of the controls showed cardiomegaly as well as alteration in the echotexture of the kidneys. 7 of them suffered proteinuria without overt CCF. Three of the controls developed hyperuricemia needing pharmacotherapy for control. All the 30 controls were stabilized on anti-hypertensives which they continue to use till the end of 15th month; on the contrary only one patient out of 30 was on therapy at this time.

Discussion

These displaced persons living under physical and mental stress, were accidentally found to be HIV +ve and followed over a period of 15 months. Although hypertension is a common ailment in this community, these people were having a normal build, but with a positive family history of hypertension and a habit of smoking started in early life. Six of them manifested with established hypertension and three with full blown stigmata of hypertension involving the heart, the kidneys and the retina and altered lipid profile needing regular antihypertensives for quite sometime. The rest also suffered labile hypertension (a term not in much vogue) and were in the pre-hypertensive state as per the JNC-7 nomenclature, for which they were prescribed, DASH and other lifestyle interventions. Their controls, on the other hand, developed full blown picture of hypertension with the involvement of heart, kidneys and vascular changes reflected in the optic fundi, needing full time anti-hypertensive therapy which they are still continuing. Although it is not necessary that all the siblings in a family with hypertension should develop the disease, but the presence of full blown disease in the siblings (18 cases) and other matched controls is a strong pointer, that the patients might have suffered similarly, had it not been for their HIV infection, with return to normal after a few months of improved habits, DASH and pharmacotherapy. It is presumed that presence of HIV Infection might have had a role to play.

Conclusions

That HIV infection affords relief in rheumatoid arthritis, has been well established and also that HIV infection as well as HAART lead to an increase in cardiovascular mortality due to dyslipidemias, insulin resistance and body fat redistribution akin to the Metabolic Syndrome (70% on autopsy in the West). Although, a paradox, few reports from the West also mentions the prophylactic effect of HIV in hypertension though no basis has yet been substantiated; a lower CD4+ count and a higher viral load being associated with a reduced risk of developing hypertension in univariate analysis in women. The mechanism though remains obscure as is the cause of essential hypertension, but perhaps some involvement of the immune system may be needed for development of essential hypertension as it is for pre-eclampsia. This study also shows a similar response wherein HIV seems to have implemented a “status-quo” on the prevalence of hypertension in these patients. Although the number of patients is small, further research on a larger population in the years to come may substantiate our results.

References

  1. Laura P. Svetkey and William L. Fan : Management of Hypertension in HIVinfected Patients (Duke University Medical Centre, 05-04-2005).
  2. Bergersen BM, Sandvik L, Dunlop O, Birkeland K, Bruun JN : Prevalence of hypertension HIV-positive patients on highly active retroviral therapy (HAART) compared with HAART-naïve and HIV-negative controls : results from a Norwegian study of 721 patients. Eur J Clin Microbiol Infect Dis. 2003 Dec; 22 (12) 731-6.
  3. Clayden P: Hypertension related to HAART in HIV-positive women. HIV i-Base, HIV Treatment Bulletin Vol 5 No 3 April 2004.
  4. Jung O, Bickel M, Ditting T, Rickerts V, Welk T, Helm EB, Staszewski S, Geiger H: Hypertension in HIV-1-infected patients and its impact on renal and cardiovascular integrity.
  5. Jerico C, Knobel H, Montero M, Sorli ML, Guelar A, Gimeno JL, Saballs P, Lopez- Colomes JL, Pedro-Botet J: Hypertension in HIV-Infected Patients: Prevalence and Related Factors.
  6. Roccella EJ et al: The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The JNC- 7 Report
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