Calcium pyrophosphate deposition disease: an independent risk factor for cardiovascular complications

A retrospective study showed that patients with calcium pyrophosphate deposition disease (CPPD) have a significantly elevated risk for all-cause mortality and major adverse cardiovascular events, independent from other cardiovascular risk factors [1].

Previous studies have already shown that patients with CPPD not only have precipitation of calcium pyrophosphate crystals in joints but also in the vasculature. While vascular calcification is implicated in the development of cardiovascular disease, studies of cardiovascular risks in CPPD are lacking. With their retrospective cohort study, Dr Maaman Bashir (Medical College of Wisconsin, USA) et al. aimed to assess the risk of cardiovascular events and all-cause mortality in patients with CPPD, compared with those without the disease. In detail, they investigated the risk of major adverse cardiovascular event (MACE) in US veterans with CPPD versus veterans without CPPD using data from the national Veterans Affairs database (2010-2014). CPPD patients (diagnosed by ICD-9 code) were age and sex-matched 1:4 with patients without the disease that served as controls. The primary outcome was any MACE, defined by ICD-9 and/or procedure codes for myocardial infarction, acute coronary syndrome, re-vascularisation, or ischaemic stroke. Secondary outcomes included individual types of MACE and all-cause mortality. As MACE was extremely uncommon in females, only male patients were included in this analysis.

In total, 24,413 male patients with CPPD were identified and were compared with 97,591 controls. MACE occurred in 2.88% of patients with CPPD and 1.10% of controls (see Figure). The incidence rate per 1,000 person-years of any MACE was nearly 3 times higher in patients with CPPD compared with controls (11.5 vs 4.3). In addition, patients with CPPD had higher all-cause mortality. The elevated cardiovascular risk remained after adjustment for traditional cardiovascular risk factors (hypertension, hyperlipidaemia, diabetes, smoking, obesity, gout, chronic kidney disease, and peripheral vascular disease). It is noteworthy that both CPPD and atherosclerotic disease may respond to IL-1 cytokine pathway antagonism suggesting hitherto unappreciated shared inflammatory pathway mechanisms [2,3].

Figure: Percentage of patients without any MACE over time in CPPD and control groups [1]

CPPD, calcium pyrophosphate deposition disease; MACE, major adverse cardiovascular event

1. 
   
   1. Bashir MZ et al. Abstract L04. ACR 2019, 9-13 November, Atlanta (GA/USA).
   2. McGonagle D, et al. Arthritis Rheum. 2008 Feb;58(2):631-3.
   3. Ridker PM, et al. N Engl J Med. 2017 Sep 21;377(12):1119-1131.

 



Posted on 4 February 202031 January 2024