Coronary artery disease affects thousands of Icelanders and is the most common cause of death in Iceland. In recent years great strides have been taken towards deeper understanding and improved treatment of this common disease, resulting in markedly improved outcomes. This evidence based review article is the first of two on coronary artery diseases. The first article will discuss the epidemiology and pathogenesis of coronary artery disease but also clinical presentation and diagnostic work-up. The second article will primarily focus on treatment of the disease including medical, interventional and surgical therapies. Both reviews are aimed at a wide readership of physicians, other health care providers and students of health sciences. Current literature will be reviewed with special focus on recent Icelandic studies.

Figure 1. Declining coronary heart disease death rates in Iceland 2006-2009. The figure is taken from The Icelandic Heart Association Statistical Handbook 2008 - Cardiovascular disease in Iceland and risk factors.

Fig. 2a - Initiation and evolution of the atherosclerotic plaque.The first step in atherogenesis is infiltration of LDL particles through the endothelial lining, especially at sites with increased permeability. Oxidative modification of LDL results in expression of adhesion molecules for leukocytes and stimulates LDL-uptake by macrophage scavenger receptors (a).

Fig. 2b. - Monocytes adhere to the activated endothelial surface, migrate into the intima and differentiate into macrophages that in addition to taking up modified LDL produce inflammatory cytokines, proteases and oxyradicals that, in turn, perpetuate the inflammation (b).

Fig. 2c. - This figure depicts the complexity of the atherosclerotic inflammation. Antigens presented by macrophages and dendritic cells trigger the activation of T-lymphocytes. Most produce Th1 cytokines that are proinflammatory, e.g. interferon γ,but regulatory T-cells are also present that produce interleukin 10 and transforming growth factor β that have anti-inflammatory and thus antiatherogenic effects (c). The figures are from reference 24 and are published with courtesy of New England Journal of Medicine.

Figure 3. Histopathologic characteristics of coronary atherosclerosis comparing thin and thick cap fibroadenomas with varying degree of luminal stenosis. The top row (A,B,C) demonstrates plaque rupture with luminal thrombosis in vessels with mild, moderate and severe luminal stenosis, respectively. The mid row (D,E,F) shows rupture prone, thin cap fibroadenomas with increasing luminal stenosis. The bottom row (G,H,I) demonstrates stable, thick cap fibroadenomas with increasing luminal stenosis shown from left to right. The figure is taken from reference nr. 27 and is published with courtesy of the Journal of the American College of Cardiology.

Figure. 4a. EKG changes of acute myocardial infarction. New left bundle branch block (left panel) or ST segment elevation in two adjacent leads (right panel) indicates occlusion of coronary artery (STEMI).

Figure 4b. EKG changes typical for Acute coronary syndromes (UAP or NSTEMI), with horizontal ST segment depression of 1 mm or more from baseline level or inverted T wave.

Fig. 5. SPECT imaging of the heart, both at reast and during excertion. Picture: Ragnar Daníelsen.

Fig. 6. Computed tomography of the left descending coronary artery, demonstrating atherosclerotic changes in the proximal (arrow) and middle parts of the artery.  

Figure 7. Cardiac enzyme elevations after acute myocardial infaction. Picture: Karl Andersen.

Table I.  Risk factors of coronary heart disease

Unchangeable risk factors

Age

Gender

Family history (nearly 60 risk variants have been identified that associate with coronary heart disease)

Modifiable risk factors

Smoking

Lipid disorders (elevated LDL-cholesterol, low HDL-cholesterol, elevated non-HDL cholesterol, elevated lipoprotein (a), elevated triglycerides)

Hypertension

Diabetes

Obstructive sleep apnoea

Sedentary life style

Coagulation factors (fibrinogen, factor VII)

Inflammatory factors (CRP, interleukin-6)

Excessive alcohol consumption

Hypothyroidism

Chronic renal failure

Psychological factors

Poverty and other adverse social conditions

Table II. The Canadian Cardiovascular Society Angina Grading Scale for the classification of severity of angina (a) and the New York Heart Association Functional Classification of heart failure (b).

Class I – Angina only during strenuous or prolonged physical activity

Class II – Slight limitation, with angina only during vigorous physical activity

Class III – Symptoms with everyday living activities, i.e., moderate limitation

Class IV – Inability to perform any activity without angina or angina at rest, i.e., severe limitation

(b)

NYHA Class	Symptoms
I	Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. shortness of breath when walking, climbing stairs etc.
II	Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
III	Marked limitation in activity due to symptoms, even during less-than-ordinary activity, e.g. walking short distances (20–100 m). Comfortable only at rest.
IV	Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients.

 

Table III. Causes of chest pain (differential diagnoses)

•         Heart

–        Coronary heart disease

–        Aortic stenosis

–        Hypertrophic cardiomyopathy

•         PericarditisVasculature

–        Aortic dissection

–        Pulmonary embolism

–        Pulmonary hypertension

•         Lungs

–        Pneumonia

–        Pleuritis

–        Tracheitis/bronchitis

–        Pneumothorax

–        Tumor

•         Mediastinitis 

– Pneumomediastinum

•         Gastrointestines

–        Esophageal reflux

–        Esophageal spasm

–        Mallory Weiss tear

–        Peptic ulcer

–        Cholecystitis/cholelithiasis

–        Pancreatitis

•         Musculoskeletal

–        Cervical disc

–        Arthritis in shoulder or neck

–        Costochondritis

–        Intercostal, pectoral, scalenius tenderness

–        Sacromial bursiti

•         Other

–        Breast pathology (inflammation, tumors etc)

–        Chest wall tumor

–        Herpes zoster