IUHS Student-2-Student USMLE Step 1 Recall

                                                Cardiovascular

                                     Ischemic Coronary Heart Disease

Angina Pectoris

angina pectoris is the term used to describe discomfort due to transient myocardial ischaemia and constitutes a clinical syndrome rather than a disease; it may occur whenever there is imbalance between myocardial oxygen supply and demand...

coronary atheroma is by for the most common cause but angina is also a feature of aortic valve disease, hypertropic cardiomyopathy and some other forms of heart disease...

Stedman's Definition of Atheroma - The lipid deposits in the intima of arteries, producing a yellow swelling on the endothelial surface; a characteristic of atherosclerosis.

central chest pain that is precipitated by exertion and promptly relieved by rest...

patients describe tightness in the chest...breathlessness is sometimes a prominent feature...the pain may radiate to the jaw and is often accompanied by discomfort in the arms, particularly the left, the wrists and sometimes the hands; the patient may also describe a feeling of heaviness or uselessness in the arms (referred pain)...

occasionally the pain is epigastric or interscapular...

symptoms tend to be worse after a meal, in the cold, and when walking uphill or into a strong wind...

the ECG may show evidence of previous myocardial infarction but is normal in most patients..occasionally there is T wave flattening or inversion in some leads, providing non-specific evidence of myocardial ischaemia or damage...

the most convincing ECG evidence of myocardial ischaemia  is obtained by demonstrating reversible ST segment depression or elevation, with or without T wave inversion, at the time the patient is experiencing symptoms...

test should stop if the patient develops significant chest pain or discomfort, a serious arrhythmia, a fall in blood pressure or marked ST segment changes...

planar or downslopping ST segment depression of 1mm or more is indicative of ischaemia, upslopping ST depression is less specific and often occurs in normal individuals...

aspirin reduces the risk of adverse events such as myocardial infarction and should be prescribed for all patients with coronary artery disease indefinitely unless it causes troublesome dyspepsia or other side-effects...

nitrates act directly on vascular smooth muscle to reduce venous and arteriolar dilatation, their beneficail effects in angina are due to a reduction in myocardial oxygen demand (lower preload and afterload) and an increase in myocardial oxygen supply (coronary vasodilatation)...

sublingual glyceryl trinitrate (GTN) is put under the tonue or crunched and retained in the mouth, will usually relieve an attack of angina in 2-3 minutes...

unwanted side effects include headaches, symptomatic hypotension, and rarely, syncope...

Prinzmetal Variant Angina

is an uncommon pattern of episodic angina that occurs at rest and has been documented to be due to coronary artery spasm...

usually there is elevation of the ST segment of the electrocardiogram, indicative of transmural ischemia...

although individuals with this form of angina may well have significant coronary atherosclerosis, the anginal attacks are unrelated to physical activity, heart rate, or blood pressure...

prinzmetal angina generally responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers...

may be associated with Thromboxane A2...

Unstable Angina

unstable angina is the term used to describe patients who present with rapidly worsening angina (crescendo angina), severe angina at rest or prolonged and severe ischaemic chest pain without ECG or enzyme evidence of significant myocardial infarction...it may present as a new phenomenon or against a background of chronic stable angina...

the culprit lesion is usually a complex ulcerated or fissured atheromatous plaque with adherent platelet-rich thrombus and local coronary artery spasm...it is important to appreciate that coronary artery thrombosis is a dynamic process whereby the obstruction may grow by thrombosis and changes in plaque morphology, sometimes leading to complete occlusion of the vessel, or regress, sometimes only temporarily, due to the effects of platelet disaggregation endogenous thrombolysis...

episodes of myocardial ischaemia are due to an abrupt reduction in coronary blood flow caused by thrombosis or spasm (supply-led ischaemia)...in contrast, stable angina is related to a fixed obstruction and usually precipitated by an increase in myocardial oxygen demand (demand-led ischaemia)...

the ECG may show ST/T wave changes including ST depression, transient ST elevation and T wave inversion...the T wave changes are sometimes prolonged...unstable angina may result in the release of specific intracellular levels of cardiac enzymes (troponin T and I) and raised levels of such enzymes indicate an adverse prognosis...

Myocardial Infarction

myocardial infarction is almost always due to the formation of occlusive thrombus at the site of rupture of an atheromatous plaque in a coronary artery...the thrombus often undergoes spontaneous lysis over the course of the next few days, although by this time irreversible myocardial damage has occurred...

without treatment the infarct-related artery remains permanently occluded in 30% of patients...many early deaths are due to ventricular fibrillation but in patients who survive the first few hours the outcome is largely determined by the extent of myocardial damage...

the process of infarction takes at least 8 hours and therefore most patients present when it is still possible to salvage myocardium and improve outcome...

pain is the cardinal symptom of myocardial infarction, but breathlessess, vomiting and collapse or syncope are common features...the pain occurs in the same sites as angina but is usually more severe and lasts longer; it is often described as a tightness, heaviness or constriction in the chest...

at its worst the pain is one of the most severe which can be experienced and the patient's expression and pallor may vividly convey the seriousness of the situation...

most patients are breathless and in some this is the only symptom...if syncope occurs it is usually due to an arrhythmia or profound hypotension...

vomiting and sinus bradycardia are often due to vagal stimulation and are particulaly common in patients with inferior myocardial infarction...

sudden death, from ventricular fibrillation or asystole, may occur immediately, and many deaths occur within the first hour...if the patient survives this most critical stage, the liability to dangerous arrhythmias remains, but diminishes as each hour goes by...the development  of caridac failure reflects the extent of myocardial damage and is the major cause of death in those who survive the first few hours of infarction...

earliest ECG change is usually ST elevation; later on there is diminution in the size of the R wave, and in transmural (full thickness) infarction a Q wave begins to develop...

one explanation for the Q wave is that the myocardial infarct acts as an 'electrical window', transmitting the changes of potential from within the ventricular cavity, and allowing the ECG to 'see' the reciprocal R wave form the other wall of the ventricle...

subsequently the T wave becomes inverted b/c of a change in ventricular repolarisation; this change persists after the ST segment has returned to normal...

subendocardial infarction causes ST/T wave changes without Q waves or prominent ST elevation; this is often accompanied by some loss of the R waves in the leads facing the infarct...

Creatine Kinase (CK)-MB - most widely used in the detection of MI...CK starts to rise 4-6 hours, and peaks 12 hours and falls to normal within 48-72 hours...

Aspartate Aminotransferase (AST) - starts to rise about 12 hours after infarction and reaches a peak on the first or second day, returning to normal within 3 or 4 days...

Lactate Dehydrogenase (LDH) - starts to rise after 12 hours, reaches a peak after 2 or 3 days and may remain elevated for a week or more; measurements of LDH are therefore appropriate when a patient presents several days after a possible infarct...

subcutaneous heparin, given in addition to oral aspirin, may prevent reinfarction after successful thrombolysis and reduce the risk of thromboembolic complications...

there is a risk of cerebral haemorrhage and other bleeding complcations...

a period of treatment with warfarin should be considered if there is persistent atrial fibrillation, evidence of extensive anterior infarction, or if echocardiography shows mobile mural thrombus, b/c these patients are at increased risk of systemic thromboembolism...

ventricular fibrillation usually occurs in about 5-10% of patients who reach hospital, and is thought to be the major cause of death in those who die before receiving medical attention...

prompt defibrillation will usually restore sinus rhythm...

moreover, the prognosis of patients who are successfully resuscitated in this way is identical to the prognosis of patients with acute myocardial infarction that is not complicated by ventricular fibrillation...

the need to recognize and treat ventricular fibrillation quickly is one of the main foundations on which the policy of acute coronary care is built...

Dressler's Syndrome

the post MI syndrome (Dressler's syndrome) is characterized by persistent fever, fibrous pericarditis and pleurisy and is probably due to autoimmunity...

the symptoms tend to occur a few weeks or even months after the infarct and othen subside after a few days; prolonged or severe symptoms may require treatment with high dose aspirin, NSAIDs, or even corticosteroids...

autoimmune pericarditis 6-8 weeks after MI...

Aortic Dissection

aortic dissection is caused by a tear in the intima of the aorta, exposing the diseased media to blood at intra-aortic pressure...the media is cleaved into two layers, creating a 'false lumen' in addition to the existing or 'true lumen'...

the dissection may compromise branches of the aorta as it spreads along its length, causing, for example, cerebral, coronary or renal ischaemia...

the false lumen may go on to rupture externally into the left pleural space or pericardium, or internally re-entering the true lumen...

loss of elastic tissue in media...

cystic medial necrosis...

may die of cardiac tamponade...

clinical presentation is usually acute, with very sudden onset of extremely severe pain in the chest and back, often starting between the shoulder blades, migrating, and frequently described as 'tearing'...

on examination there may be hypertension and asymmetry of the brachial, carotid or femoral pulses...

in type A dissection there may be signs of aortic reflux...(early diastolic murmur)...

hypertension and atherosclerosis are risk factors for aortic dissection...