Coronary heart disease: Difference between revisions

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====Plaque rupture and inflammation====
====Plaque rupture and inflammation====
Rupture of [[atherosclerosis|atherosclerotic]] plaques may cause [[acute coronary syndrome]]. Inflammation may underlay the association between elevated [[C-reactive protein]] levels and coronary heart disease.  
Rupture of [[atherosclerosis|atherosclerotic]] plaques may cause [[acute coronary syndrome]]. Inflammation may underlay the association between elevated [[C-reactive protein]] levels and coronary heart disease.
 
Surprisingly, more fatal ruptures occur on plaques that are not severely stenosed.<ref name="pmid8790027">{{cite journal| author=Mann JM, Davies MJ| title=Vulnerable plaque. Relation of characteristics to degree of stenosis in human coronary arteries. | journal=Circulation | year= 1996 | volume= 94 | issue= 5 | pages= 928-31 | pmid=8790027 | doi= | pmc= | url= }} </ref><ref name="pmid15547008">{{cite journal| author=Kolodgie FD, Virmani R, Burke AP, Farb A, Weber DK, Kutys R et al.| title=Pathologic assessment of the vulnerable human coronary plaque. | journal=Heart | year= 2004 | volume= 90 | issue= 12 | pages= 1385-91 | pmid=15547008 | doi=10.1136/hrt.2004.041798 | pmc=PMC1768577 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15547008  }} </ref><ref name="pmid10807742">{{cite journal| author=Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM| title=Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. | journal=Arterioscler Thromb Vasc Biol | year= 2000 | volume= 20 | issue= 5 | pages= 1262-75 | pmid=10807742 | doi= | pmc= | url= }} </ref>


[[Periodontal disease]] may contribute to this inflammation.<ref name="pmid18807098">{{cite journal |author=Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M |title=Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis |journal=J Gen Intern Med |volume=23 |issue=12 |pages=2079–86 |year=2008 |month=December |pmid=18807098 |doi=10.1007/s11606-008-0787-6 |url=http://dx.doi.org/10.1007/s11606-008-0787-6 |issn=}}</ref><ref name="pmid20508025">{{cite journal| author=de Oliveira C, Watt R, Hamer M| title=Toothbrushing, inflammation, and risk of cardiovascular disease: results from Scottish Health Survey. | journal=BMJ | year= 2010 | volume= 340 | issue=  | pages= c2451 | pmid=20508025  
[[Periodontal disease]] may contribute to this inflammation.<ref name="pmid18807098">{{cite journal |author=Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M |title=Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis |journal=J Gen Intern Med |volume=23 |issue=12 |pages=2079–86 |year=2008 |month=December |pmid=18807098 |doi=10.1007/s11606-008-0787-6 |url=http://dx.doi.org/10.1007/s11606-008-0787-6 |issn=}}</ref><ref name="pmid20508025">{{cite journal| author=de Oliveira C, Watt R, Hamer M| title=Toothbrushing, inflammation, and risk of cardiovascular disease: results from Scottish Health Survey. | journal=BMJ | year= 2010 | volume= 340 | issue=  | pages= c2451 | pmid=20508025  

Revision as of 07:50, 23 December 2011

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Coronary heart disease (CHD), also called coronary artery disease (CAD), is a vascular disease caused by abnormalities the arteries that supply the heart with blood (called the coronary arteries). The usual cause of coronary heart disease is atherosclerosis.

Etiology/cause

The cause and manifestation of coronary heart disease is multifactorial. About 3/4 of the risk of coronary heart disease is due to three risk factors: hypercholesterolemia (total cholesterol > 182 mg/dL [4.71 mmol/L]), hypertension (diastolic blood pressure > 90 mm Hg), and cigarette smoking.[1]

Atherosclerosis

For more information, see: Atherosclerosis.

Atherosclerosis is a degenerative disease of the arterial walls, in which the normal elastic walls of the arteries become thickened and replaced with deposits of fatty material, including cholesterol. As the walls of the affected arteries thicken, the hollow lumen at the center of each, that conduit through which oxygen enriched blood normally pulses, becomes narrower and, eventually, the flow of blood within it is decreased. With narrowing of the artery's lumen and reduced flow comes the risk of sudden occlusion of the artery, especially if the lining is abnormally roughened by deposits of irregular plaques of minerals and fats. However, the site of current stenoses does not predict the site of a subsequent myocardial infarction.[2]

About 10% of patients with chronic angina have atherosclerosis of the left main coronary artery.[3][4] In males over age 70 with definite angina, almost 50% have obstruction of the left main coronary artery.[4]

The extent of coronary obstructions can be quantified with:


Plaque rupture and inflammation

Rupture of atherosclerotic plaques may cause acute coronary syndrome. Inflammation may underlay the association between elevated C-reactive protein levels and coronary heart disease.

Surprisingly, more fatal ruptures occur on plaques that are not severely stenosed.[7][8][9]

Periodontal disease may contribute to this inflammation.[10][11] Poor oral hygiene is associated with elevated C-reactive protein and fibrinogen.[11]

Coronary vasospasm

Approximately 15% of NSTEMI and 2% of STEMI patients have no obstruction of coronary arteries and in about half of these patients, spasm of a coronary artery can be induced.[12]

Syndrome X

Cardiac syndrome X is the presence of typical angina, abnormal exercise-test results, and normal coronary arteries (including no vasospasm).[13] Syndrome X may be caused by subendocardial hypoperfusion that can be demonstrated by cardiovascular magnetic resonance imaging during the administration of adenosine.[13]

Hyperuricemia

For more information, see: Hyperuricemia.

Hyperuricemia has been proposed as contributing to coronary heart disease.

Diagnosis

History, physical examination, and risk factors

Angina pectoris, or simply angina, is the chest pain due to coronary heart disease; however, most patients do not report angina.[14] The nature of the chest pain affects the probability of underlying coronary disease.[15]

The likeilood of coronary heart disease is associated with the number of risk factors and the nature of chest pain.[16][17] A table of probabilities is available online.

The Pryor nomogram, a clinical prediction rule, can help diagnose patients with suspected chest pain in a non emergent setting.[18][19]

Cardiac stress test

For more information, see: Stress test.
Sensitivity and specificity of cardiac stress tests[20]
  Sensitivity Specificity
Exercise electrocardiography 68% 77%
Stress echocardiography 76% 88%
Myocardial perfusion imaging
thallium planar
79% 73%
Myocardial perfusion imaging
single-photon emission computed tomography (SPECT)
88% 77%
Positron emission tomography (PET), 68% 77%

The sensitivity and specificity of the various cardiac stress tests have been summarized.[20]

Exercise treadmill test

The exercise treadmill test (ETT) can help diagnose and prognose patients with suspected CHD. The likelihood of a positive treadmill test depends on the severity of the underlying coronary disease.[3] For example, 87% of patients with obstruction of the left main coronary artery will have a positive treatmill test, whereas only 57% of patients with obstructions of one or two of the other coronaries will have a positive treadmill test. The treadmill can help predict the location of coronary stenoses.[21]

Stress myocardial perfusion imaging

Stress echocardiography

Stress ventriculography

Diagnostic imaging

Several types of imaging, ranging from noninvasive to minimally invasive to invasive, can assess the degree of CHD. They include techniques using radiation transmitted through the body, imaging of radioisotopes in the body, or imaging using other mechanisms such as MRI and ultrasonography.

Most are performed before and after cardiac stress, which may be induced either by controlled exercise or pharmacologically, with drugs that stimulate the heart.

Techniques

Electron beam computed tomography

Electron beam computed tomography (EBCT) is also called ultrafast CT.

Cardiac computed tomographic angiography
For more information, see: Computed tomographic cardiac angiography.

Computed tomographic cardiac angiography has accuracy of:[22]

Single-Photon Emission-Computed Tomography
Stress echocardiography

Ultrasound-based echocardiography has long been a preferred method for assessing valvular function. cardiac output and wall movement, but, especially with the use of ultrasound-appropriate contrast media, allows better vascular visualization.

Cardiac catheterization and angiography
Magnetic resonance imaging

Magnetic resonance imaging has accuracy of:[22]

Evaluation: Coronary calcium score

Both types of computed tomography, electron beam computed tomography (EBCT) and multidetector spiral computed tomography, can measure the amount of calcium in the walls of the coronary arteries in order to diagnose coronary heart disease.

Clinical practice guidelines conflict regarding the role of the coronary calcium score. The U.S. Preventive Services Task Force[23] does not endorse using the score while the American Heart Association[24] does endorse the score. The Task Force that the best study was still compromised by using volunteers rather than being community based.[25]

Treatment

Medications

Ranolazine may increased exercise capacity and reduce symptoms[26] but not reduce cardiac events.[27]

Adrenergic beta-antagonists

Adrenergic beta-antagonists were first shown to be effective in 1981.[28]

Invasive treatments

For more information, see: myocardial revascularization.

Patient who have a left ventricular ejection fraction above 50%, no angina or their angina is controlled with medicines, do not benefit from either percutaneous transluminal coronary angioplasty (PCI)[29] or from coronary artery bypass surgery[30].

Coronary artery bypass versus percutaneous transluminal coronary angioplasty[31]
  Outcomes at 5 years Procedural related stroke
Relief of angina Repeat revascularization
CABG 84% 10% 1.2%
PTCA 79% With stents 40%
Without stents 46%
0.6%
Abbreviations:
CABG. Coronary artery bypass grafting
PTCA. Percutaneous transluminal coronary angioplasty

Regarding patients who must undergo invasive treatment, a systematic review comparing percutaneous transluminal coronary angioplasty and coronary artery bypass grafting (CABG) surgery found that CABG was more effective but was more likely to be complicated by stroke.[31]

Percutaneous cardiac intervention

For more information, see: Percutaneous transluminal coronary angioplasty.

Patient who have a stable angina and left ventricular ejection fraction above 35% do not reduce mortality from percutaneous transluminal coronary angioplasty (PCI)[32] although there is some reduction in angina for the first one to three years after procedure and few patients received stents[33][34][32]. The relief from angina, as compared to relief from medical therapy, may be reduced when evidence-based medications are used.[29]

Patients are more likely to benefit from PCI when clinical practice guidelines are followed.[35]

Stents

Meta-anlayses have found that the rate of late thrombosis was <2% between years 1 and 4.[36][37][38]

Coronary artery bypass

For more information, see: Coronary artery bypass.


Patient who have a left ventricular ejection fraction between 35 and 49 percent benefit from coronary artery bypass if they have disease of three coronary arteries.[30].

Complications

Acute coronary syndrome

For more information, see: Acute coronary syndrome.

Prognosis

See also: Vascular disease#Prognosis

Coronary calcium score

Coronary calcium score for predicting myocardial infarction or death from coronary heart disease amond 6814 persons without known cardiovascular disease[39]
Score Number of patients Hazard ratio
0 8/3409 1.0
1-100 25/1728 3.9
101-300 24/752 7.1
> 300 32/833 6.8

Both types of computed tomography, electron beam computed tomography (EBCT) and multidetector spiral computed tomography, can measure the amount of calcium in the walls of the coronary arteries in order to estimate prognosis. The calcium score improves upon using clinical risk factors for prognosticating. [39] Using clinical risk factors alone, the area under the receiver operating-characteristic curve (AUC) was 0.79 while the AUC rose to 0.83 when the calcium score was added. The clinical importance of this rise is not clear.[40]

A more recent cohort study found that the calcium score added to traditional risk factors in predicting cardiac outcomes.[41] The Net reclassification improvement was 25%.

Cardiac stress test

Various cardiac stress tests are available.

Exercise treadmill test

The exercise treadmill test (ETT) can help diagnose and prognose patients with suspected CHD. Clinical prediction rules are available to help interpret the results of the ETT. These rules are the Duke Treadmill score[42] and the newer Cleveland Clinic model[43]. The Duke score has been more extensively studied; however, in a direct comparison by the authors of the Cleveland Clinic model, the latter performed better (c-index: 0.83 vs. 0.73).[43]

The ETT adds to clinical risk factors in prediction complications. The area under the receiver-operator-characteristics-curve (AUC) for clinical data alone is 0.798 and rises to 0.857 when the ETT is added.[42]

The ETT also adds to the cardiac catheterization in prognosticating[44][45][46] although some researchers have questioned the extent of information provided by the treadmill test[17]. However, in one study among information available from cardiac catheterization, only the left ventricular ejection fraction contributed to the ETT in predicting complications[46] whereas in another study, both the left ventricular ejection fraction and the number of stenoses aided prediction[44].

Cardiac catheterization

Rates of occlusion after 4-5 years[47]
Severity of original stenosis Rate of subsequent occlusion
No stenosis 0.7%
5% to 49% 2.3%
50% to 80% 10.1%
81% to 95% 23.6%

Much research has addressed the association between severity of coronary obstructions and subsequent complications such as myocardial infarctions. Coronary obstructions are more likely to progress or occlude within 4-5 years if the obstructions are severe according to the CASS investigation.[47] 23% of subsequent occlusions were associated with a myocardial infarction. The cholesterol level or the exercise test did not improve the ability to prediction occlusion in the CASS investigation.

Surprisingly, while patients with more severe stenoses are more likely to develop occlusions predicting the exact site of furture occlusions is very difficult. Most subsequent occlusions occur in arteries that originally did not have severe stenoses and were originally not the most severely stenotic arteries in a patient.[2][48][49][50]

In addition, when occlusions develop in severely stenotic vessels, these occlusions may be less likely to cause a myocardial infarction.[50]

In summary, the concept of which coronary stenoses are vulnerable to subsequent plaque rupture and occlusion many be more important that the degree of stenosis of a vessel.[51]

Prevention

For more information, see: Vascular disease#Prevention.


References

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