Causes of death in patients with rheumatoid arthritis autopsied during a 40-year period

Kauppi

Annals of the Rheumatic Diseases

et al. 2012

Rheumatoid arthritis (RA) is a chronic inflammatory disease which is associated with an increased cardiovascular (CV) burden. Whether the risk is already present at the time of RA diagnosis remains a key area of debate. The aim of this review was to evaluate the existence of both subclinical CV changes, including endothelial dysfunction and atherosclerosis, CV risk factors, as well as CV disease manifestations such as coronary heart disease, myocardial infarction, congestive heart failure and CV death prior to RA diagnosis and during the first few years of the disease. The state of the endothelial function remains controversial in patients with newly diagnosed RA. Studies with impaired brachial artery vasodilatory responses at baseline showed a reversal of the dysfunction after 6-12 months of anti-inflammatory therapy. Morphological evidence of arterial wall atherosclerosis, measured by carotid artery intima-media thickness or the prevalence of carotid plaques, was already present during the first year following RA diagnosis. The risk of coronary heart disease and myocardial infarction is increased even prior to and, at the latest, within 1 year of the clinical onset of RA. The prevalence of hypertension was similar among patients with RA and controls. CV mortality may not increase within the first years of RA diagnosis. In conclusion, the CV risk seems to increase sooner after the RA diagnosis than previously thought. In addition to systematic CV risk assessment, patients with early RA might benefit from being targeted with stricter than conventional CV risk prevention and intervention.

Section: Overt CV Disease Manifestationsmentioning

confidence: 99%

How early in the course of rheumatoid arthritis does the excess cardiovascular risk appear?

Kauppi

Annals of the Rheumatic Diseases

et al. 2012

“…Interestingly, available pathomorphological evidence suggests that occlusive atherosclerotic coronary pathology rarely contribute to cardiovascular mortality in RA [5,6], and it is likely that systemic rheumatoid inXammation predisposes to a variety of coronary manifestations (e.g., coronaritis, vasospasm, and microvascular disease), which may destabilize atherosclerotic coronary disease in stress-associated conditions. Investigation of these conditions and their potential association with cardiovascular morbidity and mortality in RA merits further investigation.…”

Section: Introductionmentioning

confidence: 99%

Cardiac complications in rheumatoid arthritis in the absence of occlusive coronary pathology

Gasparyan

Cocco

Pandolfi³

2009

Rheumatol Int

Cardiovascular disease is the leading cause of premature mortality in patients with rheumatoid arthritis (RA). Pathophysiology of rheumatoid cardiovascular phenomenon is not fully understood, but systemic inflammation is thought to play a crucial role in the endothelial damage and accelerated course of atherosclerotic disease. Rheumatoid inflammation can also cause coronary pathology and heart failure. We present a case of transient cardiomyopathy in RA in the absence of occlusive coronary pathology, which mimics acute coronary syndrome.

“…Gastrointestinal (GI) disease is one of the most common comorbidities that can adversely affect the quality of life and the lifespan of patients with rheumatoid arthritis (RA) 1,2,3,4,5,6,7 . There is extensive research showing increased risk of upper GI disease, particularly, drug-related upper GI disease, in RA 8,9,10,11,12,13 .…”

mentioning

confidence: 99%

Increased Incidence and Impact of Upper and Lower Gastrointestinal Events in Patients with Rheumatoid Arthritis in Olmsted County, Minnesota: A Longitudinal Population-based Study

Myasoedova

Matteson²,

Talley³

et al. 2012

J Rheumatol

Objective To assess the incidence and mortality impact of upper and lower gastrointestinal (GI) events in rheumatoid arthritis (RA) compared to non-RA subjects. Methods We identified incident upper and lower GI events and estimated their incidence rates using person-year methods in a population-based incident RA cohort of residents of Olmsted County, Minnesota, USA (1987 American College of Rheumatology criteria first fulfilled between January 1, 1980, and January 1, 2008) and non-RA subjects from the same population. Results The study included 813 patients with RA and 813 non-RA subjects (mean followup 10.3 and 10.8 yrs, respectively); 68% women; mean age 55.9 yrs in both cohorts. The rate of upper GI events/100 person-years was 2.9 in RA versus 1.7 in the non-RA cohort (rate ratio 1.7, 95% CI 1.4, 2.2); for lower GI events, the rates were 2.1 in RA versus 1.4 in the non-RA cohort (rate ratio 1.5, 95% CI 1.1, 1.9). The incidence of upper GI bleed, perforation, ulcer, obstruction, and any upper GI event in RA declined over calendar time; the incidence of lower GI events remained unchanged. Exposure to glucocorticoids, prior upper GI disease, abdominal surgery, and smoking were associated with lower GI events in RA. Both upper and lower GI events were associated with increased mortality risk in RA. Conclusion There is increased risk of serious upper and lower GI events in RA compared to non-RA subjects, and increased GI-related mortality in RA. Prominent declines in incidence of upper, but not lower GI events in RA highlight the need for studies investigating lower GI disease in patients with RA.