Exploring the link between cardiovascular risk factors and manifestations in latent tuberculosis infection: a comprehensive literature review

Abstract

Background The global burden of tuberculosis (TB) and cardiovascular disease (CVD) is overt, and the prevalence of this double burden disease remains steadily rising, particularly in low- and middle-income countries. This review aims to explore the association between latent tuberculosis infection (LTBI) and the development of cardiovascular diseases and risk factors. Furthermore, we elucidated the underlying pathophysiological mechanisms that contribute to this relationship. Main body Approximately 25% of the global population carries a dormant form of tuberculosis (TB) infection. During this latent stage, certain subsets of mycobacteria actively reproduce, and recent research suggests that latent TB infection (LTBI) is connected to persistent, long-term low-grade inflammation that can potentially contribute to the development of atherosclerosis and cardiovascular disease (CVD). The presence of LTBI can be confirmed through a positive result on either a tuberculin skin test (TST) or an interferon-gamma release assay (IGRA). Several plausible explanations for the association between LTBI and CVD include increased inflammation, autoimmunity related to heat shock proteins (HSP), and the presence of pathogens within the developing atherosclerotic plaque. The most commonly observed cardiovascular events and risk factors associated with LTBI are acute myocardial infarction, coronary artery stenosis, diabetes mellitus, and hypertension. Conclusions This article highlights the critical role of LTBI in perpetuating the tuberculosis disease cycle and its association with cardiovascular risk factors. Chronic and persistent low inflammation underlined the association. Identifying high-risk LTBI patients and providing targeted preventive medication are crucial strategies for global TB eradication and interrupting transmission chains.

Effect of prior tuberculosis on cardiovascular status in perinatally HIV-1-infected adolescents

“…All regression models were adjusted for age, sex, BMI, HIV viral suppression, and exposure to protease inhibitors (PI) and nonnucleoside reverse transcriptase inhibitors (NNRTI). However, conditions (2) and (3) were not met (as outlined in Results section), i.e., there was no evidence of mediation by hsCRP, and we therefore did not proceed to test condition (4). The remainder of the analyses focused on history of TB (exposure) and its association with VAC indices using traditional statistical approaches.…”

“…1,2 Chronic infection-induced cellular and humoral immune activation and systemic inflammation may contribute to endothelial dysfunction, hypercoagulability, atherosclerosis, myocardial inflammation and fibrosis. 3,4 These pathological changes precede and characterize adverse cardiovascular events in the general population. In this regard, HIV-1 is now well recognized as an independent risk factor for CVD.…”

Latent tuberculosis infection and incident cardiovascular and non-cardiovascular death

“…From these, we estimated RMST and RMTL at 18 years for each TB exposure group, as well as their differences between the TB negative versus LTBI groups. Eighteen (18) years was chosen because it was the minimum of the longest follow-up time of the two TB sensitization groups.…”

“…Similarly, other lines of evidence have also noted association between prior tuberculosis and new onset diabetes mellitus(12), lung cancer (13), (14), Parkinson’s disease (15) and persistent neurological deficits (16), among other health impairments. In this regard, it remains to be ascertained whether latent TB infection (LTBI), at the opposite end of the immuno-pathological spectrum, may also influence these adverse outcomes, including cardiovascular morbidity and mortality (17), (18), (19).…”

“…Whilst ostensibly healthy, it may be that tuberculosis sensitized persons who have ongoing bacillary replication experience subclinical immune activation and systemic pathology leading non-specifically to future morbidity, including CVD (20), (18). A sparse and heterogenous literature reports, for example, increased odds of both prevalent and incident CVD in LTBI (21), (22), (23), (24), (25), (26).…”