Adult Kawasaki Disease: Report of Two Cases and Literature Review

Sève, P.; Stankovic, K.; Смаил, А.; Durand, D. Vital; Marchand, G.; Broussolle, C.

doi:10.1016/j.semarthrit.2005.01.012

Cited by 83 publications

(85 citation statements)

References 48 publications

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“…117 Cardiac and vascular complications (ie, myocarditis, coronary aneurysms) are the most severe manifestations of KD. 118 During the acute and subacute phases of the disease, there is activation of different proteinases, resulting in vessel wall weakening and aneurysm generation. 117 However, clinically relevant aortic involvement is rare in KD.…”

Section: Other Aortic Diseasesmentioning

confidence: 99%

Smoking and Aortic Diseases

Kakafika

Mikhailidis

2007

Circ J

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Cigarette smoking is a major cause of cardiovascular disease (CVD) and is responsible for approximately 11% of the annual total CVD deaths in the United States. 1 Smoking acts synergistically with other vascular risk factors (eg, hypertension, dyslipidaemia and diabetes) to increase vascular morbidity and mortality. 2 However, smoking has a variable magnitude of increased risk for different vascular diseases: the risk is highest for peripheral arterial disease and aortic aneurysm, and is lowest for coronary artery and cerebrovascular diseases. 2 These effects are thought to reverse after smoking cessation. The constituents of cigarette smoke with the major contribution to pathogenesis of vascular disease are nicotine, carbon monoxide, oxidant gases and polycyclic aromatic hydrocarbons. 2 Nonsmokers who are exposed to "secondhand" smoke experience on average a 30% excess risk of ischemic heart disease and nonfatal myocardial infarction. 3 Secondhand smoke exposure has been shown to activate platelets and to produce endothelial dysfunction, in both experimental animals and humans. 3 The mechanisms by which smoking causes acute cardiovascular events include endothelial dysfunction, thrombosis and inflammation.Endothelial dysfunction is an initiating event in atherogenesis, as well as a major factor in causing acute cardiovascular events. Cigarette smoking impairs flow-mediated endothelium-dependent peripheral arterial vasodilatation, an effect that is, at least partly, reversible after smoking Circulation Journal Vol.71, August 2007 cessation. 4 Smokers without atherosclerosis have coronary vasoconstrictor responses to acetylcholine that, in the presence of normal endothelium, produce vasodilatation. 5 Indeed, the oxidant chemicals of smoke degrade nitric oxide (NO) and reduce NO release, with subsequent impairment of vascular dilation and platelet function. 2 Smokers have lower than normal levels of antioxidant vitamins, reflecting their consumption in response to ongoing oxidant stress. 6 In addition, nicotine itself alters the structural and functional characteristics of vascular smooth muscle cells (VSMC) and endothelial cells. 7,8 Experimental data show that human aortic endothelial cells undergo apoptotic changes when they are exposed to cigarette smoke extracts. 9 This process may be prevented by pre-activation of NO synthase by Larginine. 9,10 Furthermore, smoking causes an increase in vascular superoxide production, which results in decreased NO bioactivity and concomitantly increases production of vasoconstrictor eicosanoids. 11 Cigarette smoke extracts, but not nicotine, also inhibit prostacyclin (PGI2: a vasodilator and inhibitor of platelet aggregation) synthesis in human, rabbit and rat vascular tissue. 12 Smoking-mediated endothelial dysfunction also results in reduced secretion of tissue plasminogen activator (tPA) 13 and increased secretion of plasminogen activator inhibitor (PAI)-1, 1 which results in impaired fibrinolysis. This acts in concert with the increased levels of tissue factor and fibrin...

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Section: Other Aortic Diseasesmentioning

confidence: 99%

Smoking and Aortic Diseases

Kakafika

Mikhailidis

2007

Circ J

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“…In addition, the prevalence of coronary artery abnormalities is higher in incomplete KD (18.4%) than in complete KD (14.2%) (7,8). There are some other known disease processes with a similar clinical presentation such as hypersensitivity drug reaction and toxic shock syndrome (9). She had no staphylococcal infection and no previous any drug intake; therefore we could rule out toxic shock syndrome and hypersensitivity drug reaction.…”

Section: A B Cmentioning

confidence: 94%

Incomplete Kawasaki Disease Manifesting as Transient Heart Failure in a Previously Healthy Adolescent

et al. 2012

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Kawasaki disease (KD) is a mucocutaneous lymph node syndrome with important cardiovascular complications which usually afflicts young children. We describe a 16-year-old woman who developed transient heart failure during the acute phase of incomplete KD. The diagnosis was based on the development of coronary aneurysms during heart failure and 2 criteria of the disease. Incomplete KD is a cause, albeit rare, of myocardial dysfunction in human adolescents. Healthcare providers should therefore be aware of the possibility of incomplete KD in patients with heart failure during the course of an acute febrile illness associated with mucocutaneous changes.

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“…9 2. Diagnostic criteria include the presence of fever lasting 5 days or more and at least four of five signs: 10 • Polymorphic rash • Erythema or desquamation of extremities • Nonexudative conjunctivitis • Injected oropharynx, fissured lips, or "strawberry tongue" • Cervical lymphadenopathy 3. Kawasaki disease may be considered in systemically ill patients meeting the diagnostic criteria above, with or without cardiac involvement, in whom viral exanthema, drug reaction, and toxic shock syndrome have been excluded.…”

Section: Clinical Teaching Pointsmentioning

confidence: 99%