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Monthly Archives: April 2017

Myocardial infarction:

Definition:

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:

  •         Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin)

AND at least one of the following:

  1.   Symptoms of ischemia
  2.   Development of pathologic Q waves on EKG
  3.   New or presumed new significant ST changes or new LBBB
  4.   Identification of an intracoronary thrombus by angiography or autopsy
  5.   Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality
  6. STEMI:
  7.  Definition:  ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads is present.
  8. Profound ST elevation or depression in multiple leads usually indicates very severe ischemia.
  9.                                    From a clinical viewpoint, the division of acute myocardial infarction into ST-segment elevation and non-ST elevation types is useful since the efficacy of acute reperfusion therapy is limited to the former group.
  10.  Etiology: STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis. Slowly developing, high-grade coronary artery stenoses do not typically precipitate STEMI because of the development of a rich collateral network over time. Instead, STEMI occurs when a coronary artery thrombus develops rapidly at a site of vascular injury. This injury is produced or facilitated by factors such as cigarette smoking, hypertension, and lipid accumulation. In most cases, STEMI occurs when the surface of an atherosclerotic plaque becomes disrupted (exposing its contents to the blood) and conditions (local or systemic) favor thrombogenesis. The amount of myocardial damage caused by coronary occlusion depends on
  11.                                the territory supplied by the affected vessel
  12.                                whether or not the vessel becomes totally occluded

iii.      the duration of coronary occlusion

  1.                                the quantity of blood supplied by collateral vessels to the affected tissue
  2.                                the demand for oxygen of the myocardium whose blood supply has been suddenly limited

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.

  1.        Signs and sxs:
  2.                           Pain is the most common presenting complaint in patients with STEMI. The pain is deep and visceral; adjectives commonly used to describe it are heavy, squeezing, and crushing. Typically, the pain involves the central portion of the chest and/or the epigastrium, and, on occasion, it radiates to the arms. Less common sites of radiation include the abdomen, back, lower jaw, and neck. It is often accompanied by weakness, sweating, nausea, vomiting, anxiety, and a sense of impending doom. The pain may commence when the patient is at rest, but when it begins during a period of exertion, it does not usually subside with cessation of activity, in contrast to angina pectoris.
  3.       Diagnostics:
  4.                              EKG:   Severe, acute ischemia lowers the resting membrane potential and shortens the duration of the action potential. Such changes cause a voltage gradient between normal and ischemic zones. As a consequence, current flows between those regions. These currents of injury are represented on the surface ECG by deviation of the ST segment. When the acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute T waves over the ischemic zone.
  5.                                    Serum Biomarkers:  Certain proteins, called serum cardiac biomarkers, are released from necrotic heart muscle after STEMI. The rate of liberation of specific proteins differs depending on their intracellular location, their molecular weight, and the local blood and lymphatic flow. Cardiac biomarkers become detectable in the peripheral blood once the capacity of the cardiac lymphatics to clear the interstitium of the infarct zone is exceeded and spillover into the venous circulation occurs. The temporal pattern of protein release is of diagnostic importance. The criteria for AMI require a rise and/or fall in cardiac biomarker values with at least one value above the 99th percentile of the upper reference limit for normal individuals.
  6.   Cardiac-specific troponin T (cTnT) and cardiac-specific troponin I (cTnI) have amino-acid sequences different from those of the skeletal muscle forms of these proteins.  These differences permitted the development of quantitative assays for cTnT and cTnI with highly specific monoclonal antibodies. Since cTnT and cTnI are not normally detectable in the blood of healthy individuals but may increase after STEMI to levels many times higher than the upper reference limit  the measurement of cTnT or cTnI is of considerable diagnostic usefulness, and they are now the preferred biochemical markers for MI.
  7.  CK rises within 4–8 h and generally returns to normal by 48–72 h. An important drawback of total CK measurement is its lack of specificity for STEMI, as CK may be elevated with skeletal muscle disease or trauma, including intramuscular injection. The MB isoenzyme of CK has the advantage over total CK that it is not present in significant concentrations in extracardiac tissue and, therefore, is considerably more specific. However, cardiac surgery, myocarditis, and electrical cardioversion often result in elevated serum levels of the MB isoenzyme.

 

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

  1.  Treatment:

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.

MONA:

  1.   M:  Morphine may be given for the relief of chest pain in the setting of acute myocardial infarction. We generally reserve its use for patients with an unacceptable level of pain, due to evidence of worse outcomes in patients receiving the drug. We give intravenous morphine sulfate at an initial dose of 2 to 4 mg, with increments of 2 to 8 mg repeated at 5- to 15-minute intervals.
  2.   O:   Oxygen, when hypoxemia is present, O2 should be administered by nasal prongs or face mask (2–4 L/min) for the first 6–12 h after infarction.
  3.   N:  Nitrates, intravenous nitroglycerin is useful in patients with persistent chest pain after three sublingual nitroglycerin tablets, as well as in patients with hypertension or heart failure. Nitrates must be used with caution or avoided in settings in which hypotension is likely or could result in serious hemodynamic decompensation, such as right ventricular infarction or severe aortic stenosis. In addition, nitrates are contraindicated in patients who have taken a phosphodiesterase inhibitor for erectile dysfunction (or pulmonary hypertension) within the previous 24 hours.
  4.   A:  Aspirin, There is strong evidence to support the early initiation of dual antiplatelet therapy with aspirin and a platelet P2Y12 receptor blocker, irrespective of treatment strategy (fibrinolysis, PCI, or medical therapy), in patients with acute-STEMI.

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:

  1.  The first change may be a hyperacute T wave. It is tall, peaked, and symmetric (the normal T wave is asymmetric with an upstroke that is slower than the downstroke) in at least two contiguous leads.
  2.  Initially, there is elevation of the J point and the ST segment retains its concave configuration but may become convex or rounded upward.
  3.   Over time, the ST-segment elevation becomes more pronounced and the ST segment changes its morphology, becoming more convex or rounded upward.
  4.   The ST segment eventually merges with the T wave and the ST-segment and T wave become indistinguishable. The QRS-T complex can actually resemble a monophasic action potential. This is a “current of injury” or so-called “tombstone” pattern. Reciprocal ST-segment depressions are usually observed in other leads.
  5.   The ST-segment returns to baseline, an initial Q wave develops, and there is a loss of R wave amplitude. When the ST segment elevation persists for greater than three weeks after the event, a ventricular aneurysm in the area may be suspected.
  6.   The T wave becomes inverted and it may remain inverted or return to upright
  7.   Over time, there is continued evolution of ECG changes. The R wave amplitude becomes markedly reduced, the Q wave deepens, and the T wave remains inverted or becomes positive. These changes generally occur within the first two weeks after the event; however, in some patients, they occur within a few hours of presentation.
  8.   LOCATION OF ST CHANGES IN RELATION TO LOCATION OF INFARCT:

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:

  1.        V1-V2 – Anteroseptal
  2.       V3-V4 – Anteroapical
  3.        V5-V6 – Anterolateral
  4.       I, aVL – Lateral
  5.       II, III, aVF – Inferior
  6.       Acute Anterior Wall MI:  An acute anterior wall MI presents with the changes in some or all of the precordial chest leads V1 to V6. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting most often as depressions of the ST segments in the inferior leads (II, III, and aVF). Reciprocal changes are actually the same ST segment shifts as seen from a different angle or direction.
  7.   Anteroseptal MI:  An acute anteroseptal MI presents with the changes in leads V1 to V2. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segments in the inferior (II, II, aVF) or lateral leads (I, aVL, V5, and V6).
  8.   Anterioapical wall MI:  An acute anteroapical MI presents with the changes in leads V3 and V4. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF).
  9.  Anterolateral wall MI :   An acute anterolateral MI presents with the changes in leads V5 and V6, often in association with changes in leads I and aVL (waveform 6). Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as depressions of the ST segment in the inferior leads (II, III, aVF), and in some cases in leads V1 and V2.
  10.  Lateral wall MI:   An acute lateral MI presents with the changes confined to leads I and aVL (waveform 7). Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting as ST segment depressions in the inferior leads (II, III, and aVF) or leads V1 and V2.
  11.  Inferior wall MI – An acute inferior wall MI presents with the changes in leads II, III, and aVF. Reciprocal ECG changes occasionally are observed during the initial period of the acute infarction, presenting with ST segment depressions in leads I and aVL. The ST segment depression in the precordial leads V1 to V2 may be reciprocal, but more likely represents true posterior wall involvement (which may be diagnosed by ST elevation in leads V7 to V9) [4]. In addition, there may be the presence of ST elevation in the precordial chest leads V1 to V2. Involvement of the right ventricle may occur with an inferior wall MI and is confirmed by the presence of ST segment elevation in V3R and V4R. The duration of ST elevation in the right precordial leads may be shorter compared to the inferior leads, and, therefore, a right-sided ECG should be obtained as soon as possible after inferior wall ST elevation is noted.
  12.  Posterior wall MI — An acute posterior wall transmural MI reflecting left circumflex coronary artery involvement may be missed on a typical ECG. Posterior lead ECG (leads V7 to V9) should be completed if there is a high degree of suspicion or if ST depression is present in V1 to V3. The criteria for ST elevation in leads V7 to V9 are ≥0.05 mV in men over 40 years and women and ST elevation of ≥0.1 mV for men <40 years.

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

Summary of Major Recommendations for the Treatment of Blood Cholesterol to Reduce ASCVD Risk in Adults

Encourage heart-healthy lifestyle habits for all individuals
Initiate or continue appropriate intensity of statin therapy
Clinical ASCVD*
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-, Moderate-, and Low-Intensity Statin Therapy (Used in the RCTs Reviewed by the Expert Panel)*

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

 

Flow Chart for treatment

Major Recommendations for Statin Therapy for ASCVD Prevention


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