acute coronary syndrome
Acute coronary syndrome (ACS) refers to clinical symptoms compatible with acute myocardial ischemia and includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI).
Unstable angina (UA) is characterized by ischemic chest pain occurring at rest or with minimal exertion, rapid deterioration of previously stable angina, or new onset severe ischemic chest pain of less than one month’s duration. Unstable angina is caused by an imbalance between myocardial oxygen supply and demand but is not relieved by rest as with stable angina. ECG findings in unstable angina vary from a normal ECG to changes of ST-segment depression and/or T-wave inversion. Importantly, in unstable angina, cardiac markers of injury (e.g., troponin) remain within the normal range.
Myocardial infarctions are divided into 2 groups: NSTEMI and STEMI. Although patient presentation is similar, the pathogenesis and ECG findings are different.
STEMI and NSTEMI
The diagnosis of both STEMI and NSTEMI is made by elevation of cardiac markers of injury, usually troponin. The ECG findings in NSTEMI vary from no apparent change to ST-segment depressions and/or T-wave inversions. STEMI differs from NSTEMI in ECG findings of STsegment elevation that result from transmural ischemia/injury. It is important to differentiate between NSTEMI and STEMI because intervention with fibrinolytic therapy or percutaneous coronary intervention (PCI) to open the occluded vessel improves outcomes in STEMI.
types of MI
• Type 1: Spontaneous MI related to atherosclerotic plaque rupture, ulceration, fissuring, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocytes necrosis. The patient may have underlying severe CAD but on occasion nonobstructive or no CAD.
• Type 2: Myocardial infarction secondary to an ischemic imbalance. In instances of myocardial injury with necrosis where a condition other than CAD contributes to animbalance between myocardial oxygen supply and/or demand, e.g. coronary endothelial dysfunction, coronary artery spasm, tachy-brady-arrhythmias, anemia, respiratory failure, hypotension or hypertension.
• Type 3 is MI resulting in death when biomarkers are unavailable.
• Type 4a is MI related to PCI.
• Type 4 b is MI related to stent thrombosis.
• Type 5 is MI related to CABG.
Typical Progression of Coronary Atherosclerosis
As the plaque burden increases, the atherosclerotic mass tends to stay external to the lumen, which allows the diameter of the lumen to be maintained; this is known as the Glagov effect, or positive remodeling.1 As plaque encroaches into the lumen, the coronary artery diameter decreases. Myocardial ischemia results from a discordant ratio of coronary blood supply to myocardial oxygen consumption. Luminal narrowing of more than 65 to 75 percent may result in transient ischemia and angina. In acute coronary syndromes, vulnerable plaque is a more important factor than is the degree of stenosis; acute coronary events result from ulceration or erosion of the fibrous cap, with subsequent intraluminal thrombosis. Vulnerable plaque within the vessel wall may not be obstructive and thus may remain clinically silent until it causes rupture and associated consequences.
Only a minority of U.S. hospitals are capable of performing primary percutaneous coronary intervention (PCI). Delay in time to reperfusion, door-to balloon after hospital arrival is associated with a higher adjusted risk of in-hospital mortality. For patients with STEMI presenting to a PCI-capable hospital, primary PCI should be accomplished within 90 minutes. For patients presenting to a non–PCI-capable hospital a decision must be made about transfer or employment of fibrinolytic therapy
analgesics in anticipation of PCI
Morphine sulfate is the drug of choice for pain relief in patients with STEMI, especially those whose course is complicated by acute pulmonary edema. It can alleviate the work of breathing, reduce anxiety, and favorably affect ventricular loading conditions
NSAIDs and COX 2 inhibitors in anticipation of PCI
Epidemiological studies and retrospective analyses of RCTs have suggested that nonsteroidal anti-inflammatory drugs and selective cyclooxygenase II enzyme (COX-2) inhibitors may be associated with an increased risk of death, reinfarction, cardiac rupture, hypertension, renal insufficiency, and HF. Nonsteroidal anti-inflammatory drugs and COX-2 inhibitors are contraindicated in patients with STEMI. They should not be initiated in the acute phase and should be discontinued in patients using them before hospitalization
oxygen in anticipation of PCI
Few data exist to support or refute the value of the routine use of oxygen in the acute phase of STEMI. The concern with oxygen for normoxic patients is that it may cause coronary constriction.
ANTIPLATELET THERAPY IN SUPPORT OF PRIMARY PCI - aspirin
162 to 325 mg should be given before primary PCI. After PCI, aspirin should be continued indefinitely. The maintence dose is 81 mg daily.
ANTIPLATELET THERAPY IN SUPPORT OF PRIMARY PCI - clopidogrel
should be given as early as possible or at time of primary PCI to patients with STEMI. The drug should be given for 1 year to patients with STEMI who receive a bare metal stent (BMS) or drug eluting stent (DES). Clopidogrel plus aspirin comprises dual antiplatelet therapy (DAPT). With DES DAPT is continued beyond one year. DAPT carries the risk of intracerebral hemorrhage especially in those with prior history of stroke.
ANTIPLATELET THERAPY IN SUPPORT OF PRIMARY PCI - abciximab
to inhibit the platelet GpIIb/IIIa receptor.
ANTIPLATELET THERAPY IN SUPPORT OF PRIMARY PCI - bivalirudin
is used by the interventional cardiologists.
Unfractionated heparin (UHF) or enoxaparin but not fondaparinux. The heparin will limit the participation of the clotting cascade in thrombus development and afford VTE prophylaxis. The interventional procedures require heparin anticoagulation.
routine medical therapy
Oral beta blockers (metoprolol succinate) should be initiated in the first 24 hours in patients with STEMI who do not have any of the following:
• Signs of HF
• Evidence of a low output state
• Increased risk for cardiogenic shock, or other contraindications to use oforal beta blockers (PR interval more than 0.24 seconds, second- or third-degree heart block, active asthma, or reactive airways disease)
Beta blockers should be continued during and after hospitalization for all patients with STEMI and with no contraindications to their use. It is reasonable to administer intravenous beta blockers at the time of presentation to patients with STEMI and no contraindications to their use who are hypertensive or have ongoing ischemia.
RAAS ACE inhibitors
An angiotensin-converting enzyme (ACE) inhibitor (Benazepril) should be administered within the first 24 hours to all patients with STEMI with anterior location, HF, or ejection fraction (EF) less than or equal to 0.40, unless contraindicated.
ACE inhibitors are reasonable for all patients with STEMI and no contraindications to their use.
Oral ACE inhibitors reduce fatal and nonfatal major cardiovascular events in patients with STEMI. Their protective effects have been demonstrated independent of the use of other pharmacotherapies (i.e., fibrinolytics, aspirin, and beta blockers). The magnitude of clinical benefit is greatest in high-risk patient subgroups (i.e., anterior MI, EF 0.40, HF, prior MI, and tachycardia).
Demonstration of an early benefit (within the first 24 hours) supports the prompt use of these agents in patients without existing contraindications (hypotension, shock, bilateral renal artery stenosis or history of worsening of renal function with ACE inhibitor/ARB exposure, renal failure, or drug allergy).
RAAS - ARBs
An angiotensin receptor blocker (ARB), losartan, should be given to patients with STEMI who have indications for but are intolerant of ACE inhibitors
RAAS - aldosterone antagonist
An aldosterone antagonist, spironolactone, should be given to patients with STEMI and no contraindications who are already receiving an ACE inhibitor and beta blocker and who have an EF less than or equal to 0.40 and either symptomatic HF or diabetes mellitus. Early initiation of the drug significantly reduces the rates of all-cause mortality, sudden cardiac death (SCD), and cardiovascular mortality/hospitalization, whereas initiation after 7 days has no significant effect on outcomes.
Treatment with statins in patients stabilized after an ACS, including STEMI, lowers the risk of coronary heart disease death, recurrent MI, stroke, and the need for coronary revascularization. More intensive statin therapy, compared with less intensive therapy, appears to be associated with an additional lowering of nonfatal clinical endpoints.
women and STEMI
• 30% of patients with STEMI
• Female sex a strong predictor of failure to receive reperfusion therapy
• Female sex was a strong independent predictor of failure to receive reperfusiontherapy among patients who had no contraindications
• Present later than men after symptom onset and with atypical symptoms
• Have longer door-to –fibrinolytic time or door to balloontime
• Less often receive aspirin or beta-blockers within 24 hours ofpresentation