According to the third universal definition (released in 2012 by theESC/ACCF/AHA/WHF), any one of the following criteria meets the diagnosis of MI:
AND at least one of the following:
iii. the duration of coronary occlusion
Vi. endogenous factors that can produce early spontaneous lysis of the occlusive thrombus
vii. the adequacy of myocardial perfusion in the infarct zone when flow is restored in the occluded epicardial coronary artery.
iii. Imaging: Abnormalities of wall motion on two-dimensional echocardiography are almost universally present. Although acute STEMI cannot be distinguished from an old myocardial scar or from acute severe ischemia by echocardiography, the ease and safety of the procedure make its use appealing as a screening tool in the Emergency Department setting. When the ECG is not diagnostic of STEMI, early detection of the presence or absence of wall motion abnormalities by echocardiography can aid in management decisions, such as whether the patient should receive reperfusion therapy
INITIAL THERAPY — The patient with acute ST elevation myocardial infarction (STEMI) should have continuous cardiac monitoring, oxygen, and intravenous access. Therapy should be started to relieve ischemic pain, stabilize hemodynamic status, and reduce ischemia while the patient is being assessed as a candidate for fibrinolysis or primary percutaneous coronary intervention (PCI), with a goal of initiating PCI within 120 min of first medical contact.. Other routine hospital measures include anxiolytics, serial electrocardiograms, and blood pressure monitoring.
STEMI EKG Changes:
The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. The findings depend on several key factors: the nature of the process (reversible [i.e., ischemia] versus irreversible [i.e., infarction]), the duration (acute versus chronic), the extent (transmural versus subendocardial), and localization (anterior versus inferoposterior), as well as the presence of other underlying abnormalities (ventricular hypertrophy, conduction defects).
Acute ischemia causes a current of injury. With predominant subendocardial ischemia (A), the resultant ST vector will be directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. With ischemia involving the outer ventricular layer (B) (transmural or epicardial injury), the ST vector will be directed outward. Overlying leads will record ST elevation.
ST-elevation MI evolution — The classic (but not invariable) sequence of ECG changes in patients with STEMI is as follows:
ST-segment elevation, associated with epicardial coronary vasospasm or actual occlusion, is a relatively specific sign of acute transmural ischemia. ST-T wave abnormalities that are suggestive of acute myocardial ischemia in the earliest phase of ST elevation MI are usually localized to those leads that reflect the involved regions of the myocardium:
Daytime Functioning: Sleep apnea can be a cause for daytime sleepiness and may cause difficulties in thinking clearly. In turn, this can lead to an increase in errors throughout the day and result in accidents being made. On average, motor vehicle crashes are two to three times more common in those who suffer from sleep apnea. In addition, those with sleep apnea are twice as likely to suffer from depression as those who do not have sleep apnea.
Cardiovascular Risk: Those who have sleep apnea are at an increased risk for various cardiovascular illnesses, such as systemic hypertension, pulmonary hypertension, coronary artery disease, cardiac arrhythmias, heart failure, and stroke.
Systemic Risk: Sleep apnea has been found to increase the risk of individuals developing type 2 diabetes among the general population. In a study that followed 8600 individuals with suspected sleep apnea, it was found that there was about a 30% higher risk of developing diabetes among those who had sleep apnea. In addition, sleep apnea has been associated with increased glucose, triglycerides, inflammation, arterial stiffness, atherosclerosis, and nonalcoholic fatty liver disease.
Overall, sleep apnea has been found to be a large contributing factor to poor health and adverse outcomes.
ACC Cholesterol Guidelines
|Encourage heart-healthy lifestyle habits for all individuals|
|Initiate or continue appropriate intensity of statin therapy|
|Age ≤ 75 years and no safety concerns: high-intensity statin (COE = I; LOE = A)|
|Age > 75 years or safety concerns: moderate-intensity statin (COE = I; LOE = A)|
|Primary prevention: primary LDL-C ≥ 190 mg per dL (4.92 mmol per L)|
|Rule out secondary causes of hyperlipidemia (see Table 6 in full guideline)|
|Age ≥ 21 years: high-intensity statin (COE = I; LOE = B)|
|Achieve at least a 50% reduction in LDL-C (COE = IIa; LOE = B)|
|Consider LDL-C–lowering nonstatin therapy to further reduce LDL-C (COE = IIb; LOE = C)|
|Primary prevention: persons 40 to 75 years of age with diabetes mellitus and with LDL-C of 70 to 189 mg per dL (1.81 to 4.90 mmol per L)|
|Moderate-intensity statin (COE = I; LOE = A)|
|Consider high-intensity statin when ≥ 7.5% 10-year ASCVD risk using the Pooled Cohort Equations† (COE = IIa; LOE = B)|
|Primary prevention: persons 40 to 75 years of age without diabetes and with LDL-C of 70 to 189 mg per dL|
|Estimate 10-year ASCVD risk using the risk calculator based on the Pooled Cohort Equations† in those not receiving a statin; estimate risk every 4 to 6 years (COE = I; LOE = B)|
|To determine whether to initiate a statin, engage in a clinician-patient discussion of the potential for ASCVD risk reduction, adverse effects, drug-drug interactions, and patient preferences (COE = IIa; LOE = C)|
|Reemphasize heart-healthy lifestyle habits and address other risk factors|
|• ≥ 7.5% 10-year ASCVD risk: moderate- or high-intensity statin (COE = I; LOE = A)|
|• 5% to < 7.5% 10-year ASCVD risk: consider moderate-intensity statin (COE = IIa; LOE = B)|
|• Other factors may be considered‡: LDL-C ≥ 160 mg per dL (4.14 mmol per L), family history of premature cardiovascular disease, high-sensitivity C-reactive protein ≥ 2 mg per L (19.05 nmol per L), coronary artery calcium score ≥ 300 Agatston units, ankle-brachial index < 0.9, or elevated lifetime ASCVD risk (COE = IIb; LOE = C)|
|Primary prevention when LDL-C < 190 mg per dL and age < 40 or > 75 years, or < 5% 10-year ASCVD risk|
|Statin therapy may be considered in select individuals‡ (COE = IIb; LOE = C)|
|Statin therapy is not routinely recommended for individuals with New York Heart Association class II to IV heart failure or who are receiving maintenance hemodialysis|
|Regularly monitor adherence to lifestyle and drug therapy with lipid and safety assessments|
|Assess adherence, response to therapy, and adverse effects within 4 to 12 weeks following statin initiation or change in therapy (COE = I; LOE = A)|
|Measure fasting lipid levels (COE = I; LOE = A)|
|Do not routinely monitor alanine transaminase or creatine kinase levels unless symptomatic (COE = IIa; LOE = C)|
|Screen and treat type 2 diabetes according to current practice guidelines; heart-healthy lifestyle habits should be encouraged to prevent progression to diabetes (COE = I; LOE = B)|
|Anticipated therapeutic response: approximately ≥ 50% reduction in LDL-C from baseline for high-intensity statin and 30% to < 50% for moderate-intensity statin (COE = IIa; LOE = B)|
|• Insufficient evidence for LDL-C or non–HDL-C treatment targets from RCTs|
|• For those with unknown baseline LDL-C, an LDL-C < 100 mg per dL (2.59 mmol per L) was observed in RCTs of high-intensity statin therapy|
|Less than anticipated therapeutic response:|
|• Reinforce improved adherence to lifestyle and drug therapy (COE = I; LOE = A)|
|• Evaluate for secondary causes of hyperlipidemia if indicated (see Table 6 in full guideline) (COE = I; LOE = A)|
|• Increase statin intensity, or if on maximally tolerated statin intensity, consider addition of nonstatin therapy in select high-risk individuals§ (COE = IIb; LOE = C)|
|Regularly monitor adherence to lifestyle and drug therapy every 3 to 12 months after adherence has been established; continue assessment of adherence for optimal ASCVD risk reduction and safety (COE = I; LOE = A)|
|In individuals intolerant of the recommended intensity of statin therapy, use the maximally tolerated intensity of statin (COE = I; LOE = B)|
|If there are muscle or other symptoms, establish that they are related to the statin (COE = IIa; LOE = B)|
|For specific recommendations on managing muscle symptoms, see Table 8 in full guideline|
|HIGH INTENSITY||MODERATE INTENSITY||LOW INTENSITY|
|Daily dosage lowers LDL-C by approximately ≥ 50% on average||Daily dosage lowers LDL-C by approximately 30% to 50% on average||Daily dosage lowers LDL-C by < 30% average|
|Atorvastatin (Lipitor), 40†to 80 mg||Atorvastatin, 10 (20) mg||Simvastatin, 10 mg|
|Rosuvastatin (Crestor), 20(40) mg||Rosuvastatin, (5) 10 mg||Pravastatin, 10 to 20 mg|
|Simvastatin (Zocor), 20 to 40 mg‡||Lovastatin, 20 mg|
|Pravastatin (Pravachol), 40(80) mg||Fluvastatin, 20 to 40 mg|
|Lovastatin (Mevacor), 40 mg||Pitavastatin, 1 mg|
|Fluvastatin XL (Lescol XL), 80 mg|
|Fluvastatin, 40 mg twice daily|
|Pitavastatin (Livalo), 2 to 4 mg|
Major Recommendations for Statin Therapy for ASCVD Prevention