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 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper on periodontal disease as a potential risk factor for systemic diseases was prepared by the Research, Science and Therapy Committee of The American Academy of Periodontology. It is intended to provide information regarding the role of periodontal disease in systemic diseases, including bacteremia, infective endocarditis, cardiovascular disease and atherosclerosis, prosthetic device infection, diabetes mellitus, respiratory diseases, and adverse pregnancy outcomes.
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PMID:Position paper of The American Academy of Periodontology: periodontal disease as a potential risk factor for systemic diseases. 970 64

Oral bacteria exhibit highly specific adherence mechanisms and as a result they colonize and cause disease principally in the oral cavity. Oral pathogens, however, can produce systemic disease and are known causative agents of infective endocarditis. Recent studies have revealed that periodontal disease per se is also a statistically significant risk factor for cardiovascular disease. A link between the two diseases is the secretion and systemic appearance in periodontitis of pro-inflammatory cytokines capable of eliciting effects associated with atherosclerosis and coronary heart disease.
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PMID:Oral pathogens: from dental plaque to cardiac disease. 1006 62

A growing amount of epidemiologic, experimental, and clinical evidence has linked infection as a risk factor to variousatherosclerotic diseases including acute myocardial infarction and cerebral infarction. Bacteremic infections with and without endocarditis carry a high risk for both stroke and acute myocardial infarction. During the last decade, chronic bacterial infections such as Chlamydia pneumoniae and dental infections have been associated as risk factors for various atherosclerotic diseases. These chronic bacterial infections are risk factors for acute cardiovascular events, but they may also have some role in the etiopathogenesis of atherosclerotic process itself. There are many known mechanisms that might explain the observed association of infection and atherosclerotic diseases, but it is probable that these mechanisms are complex and multifactorial and probably differ from infection to infection and from patient to patient. Infection theory is by no means against classic risk factor theory in the etiopathogenesis of atherosclerosis. Infection may also act as a synergistic risk factor together with classic risk factors in the development of various atherosclerotic diseases.
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PMID:Role of infections in atherosclerosis. 1053 42

Coronary artery fistulas in structurally normal hearts are rare. The natural history of these lesions depends on their size and can cause congestive heart failure, infective endocarditis, ischemia, or accelerated atherosclerosis. These fistulas are usually closed either in the catheterization laboratory or surgically. This case demonstrates the prenatal diagnosis of a left coronary to right ventricular fistula and documents its natural history to spontaneous closure by 1 year of age. This may help confirm the rationale of observation rather than closure of small fistulas in selected cases of patients without symptoms.
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PMID:Diagnosis of a left coronary artery to right ventricular fistula with progression to spontaneous closure. 1070 71

Attributes of Chlamydia pneumoniae of potential importance to a relationship with atherosclerosis are described. Among these are that C. pneumoniae is not new. It is unique. It is a pathogen with which everyone is infected, and it is difficult to treat. It causes immunopathology, myocarditis, and endocarditis and chronicity is a hallmark of Chlamydia infection. Current knowledge of the relation of C. pneumoniae and atherosclerosis comes from observational (e.g., seroepidemiology and tissue studies) and experimental studies. The limitations of the serologic studies of chronic infection are noted as is the conclusive demonstration of an association of C. pneumoniae and atherosclerosis by the repeated and frequent finding of the organism in atherosclerotic tissue. Experimental studies are needed to determine if the association is causal. Such studies should include animal models, basic mechanisms, and secondary prevention antibiotic treatment trials.
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PMID:Background and current knowledge of Chlamydia pneumoniae and atherosclerosis. 1083 24

A coronary arteriovenous fistula is a congenital or acquired coronary artery anomaly in which blood is shunted into a cardiac chamber, great vessel or other structure, superceding the myocardial capillary network. The clinical presentation may be heralded by the development of dyspnea, congestive heart failure, angina, endocarditis, dysrhythmias or myocardial infarction. The authors describe a left to right coronary artery to coronary sinus shunt that produced an elevation in right atrial pressure during exercise and thereby opened a patent foramen ovale and manifested as exercise-induced desaturation. Although noninvasive imaging may facilitate the diagnosis and identification of the origin and insertion of coronary arteriovenous fistulae, cardiac catheterization is necessary for the precise delineation of coronary anatomy, and to show the presence of concomitant atherosclerosis and structural anomalies. Possible therapeutic options in the management of coronary arteriovenous malformations include transcatheter embolization, surgical correction or expectant management.
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PMID:Massive congenital coronary arteriovenous malformation presenting with exertional dyspnea and desaturation in an adult: a case report and review of the literature. 1117 19

With the advent of more effective therapies for human immunodeficiency virus (HIV) infection, HIV-infected patients are living longer and cardiovascular disease is becoming more obvious in this population. Patients with HIV infection represent one of the most rapidly developing groups with cardiovascular disease globally. Cardiovascular disease complicating HIV infection is likely to contribute to burgeoning healthcare costs. Pericarditis, myocarditis, cardiomyopathy, atherosclerotic coronary vasculopathy, arterial aneurysms, pulmonary hypertension, and endocarditis occur with increased frequency in these patients. Pericardial tamponade, dilated cardiomyopathy, endocarditis, and vasculopathy can lead to fatal outcomes in this population. The advent of cardiomyopathy heralds a very poor prognosis in patients infected with HIV. Coronary vasculopathy without obvious risk factors can lead to myocardial ischemia in young patients infected with the virus. Moreover, the protease inhibitors used to treat HIV infection induce a syndrome of lipodystrophy and dyslipidemia that may be associated with accelerated atherosclerosis as well as insulin resistance. All these factors contribute to increased cardiovascular morbidity and mortality in the HIV-infected population. HIV infection, opportunistic infections, secreted viral proteins such as gp120 (envelope protein) or Tat (transactivator of viral transcription), and cytokines elaborated during the course of HIV infection of the immune system all contribute to pathogenesis of these disorders. Further basic and clinical studies are required to understand the pathogenesis of cardiovascular complications and develop appropriate management strategies for these patients.
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PMID:The cardiovascular and metabolic complications of HIV infection. 1117 4

At immunoproductive processes in endothelium of patients with coronary atherosclerosis and endocarditis a phase dynamics of innate immunity represented by polytypic Ca(2+)-dependent autoprecipitating proteins of nonclonal recognition of surface cell membrane components (CMC) have been revealed. In case of coronary atherosclerosis the organism reaction to expressed CMC is manifested basically by intensified synthesis of cathodic complement-C3-similar autoprecipitin, but in case of endocarditis--by consumption of one with formation of anodic autoprecipitin and by intensified synthesis of autoprecipitating immunoglobulin G. These membranotropic autoimmune reactions are identical with the organism reactions to alien (heterologous) agents and differentially participate in development both of basic disease and perioperational complications after cardiac operations using trans- and implants, hence, they should be taken into account during membrane-stabilising and immunocorrecting therapy of recipients.
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PMID:[Autoimmune processes and biocompatibility in local damage of endothelium of the heart and its vessels]. 1142 71

An occlusive thrombus in the coronary arteries is the critical pathological event that immediately precedes most cases of myocardial infarction. Often the thrombus originates with a bleed from a fissured atheroma. Atheroma formation, therefore, creates risk of thrombosis; asymptomatic episodes of thrombosis and healing contribute to the pathogenesis of atherosclerosis and the development of atherosclerotic plaques. Based largely on in vitro and animal model evidence, infectious agents and their products can activate the coagulation cascade enzymatically or by up-regulating tissue factor. By initiating a procoagulant response, infectious agents can indirectly trigger a prothrombotic response. Alternatively, some microbes can directly trigger platelet aggregation in vitro and in animal models, suggesting direct prothrombotic potential in human cardiovascular disease. Activation of coagulation and thrombosis characterizes the pathological response to infectious agents in human disseminated intravascular coagulation and infective endocarditis. Given the underlying biological plausibility, the cumulative lifetime burden of chronic pathogens may be expected to create risk of atherosclerosis and thrombosis, and, indirectly, signs of cardiovascular disease.
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PMID:Coagulation and thrombosis in cardiovascular disease: plausible contributions of infectious agents. 1188 59

Splenic arterial aneurysms (SAA) are rare and are usually atherosclerotic and/or related to pregnancy. Because pregnancy is the most important predisposing factor, the strong predilection of SAA for women is not surprising. The authors report a case of SAA rupture in a man with chronic pancreatitis as the predisposing factor. A 56-year-old man with abdominal pain and hematemesis was resuscitated and underwent endoscopy, but he died 18 hours later of massive hematemesis before definitive surgery could be carried out. At autopsy, there was chronic pancreatitis with fibrous adhesions tethering the tail of the pancreas, spleen, and posterior wall of the stomach together. The SAA was indented into the posterior wall of the stomach, into which it had ruptured from without. He also had alcoholic cirrhosis but no esophageal varices or conventional gastric ulcers. Other important predisposing factors such as abdominal trauma, infective endocarditis, polyarteritis nodosa, and segmental medial arteriopathy were absent. Histologic examination confirmed the rupture of the SAA. The SAA had Monckeberg medial calcinosis but little evidence of atherosclerosis. The well-documented complications of acute and chronic pancreatitis include shock, abscess, pseudocyst formation, and duodenal obstruction. This report describes the rare complication of SAA rupture, which may be fatal.
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PMID:Fatal splenic arterial aneurysmal rupture associated with chronic pancreatitis. 1219 58


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