Question

- STEMI vs NSTEMI; diagnosis, clinical manifestations (including atypical manifestations

in women, elderly, and diabetics), serum markers, basic treatment; possible sequelae

- scar tissue formation and its effects on cardiac muscle

- effect of MI on CO, compensatory mechanisms

- sudden cardiac arrest: description, type of associated arrhythmia

- endocardial and valvular diseases: prolapse vs stenosis vs regurgitation – how do these affect blood flow?

Answer 1

Ans) History, ECG, and cardiac biomarkers are the mainstays in the evaluation. An ECG should be performed as soon as possible in patients presenting with chest pain or those with a concern for ACS. A normal ECG does not exclude ACS and NSTEMI. ST-elevation or anterior ST depression should be considered a STEMI until proven otherwise and treated as such. Findings suggestive of NSTEMI include transient ST elevation, ST depression, or new T wave inversions. ECG should be repeated at predetermined intervals or if symptoms return.

Cardiac troponin is the cardiac biomarker of choice. Troponin is more specific and more sensitive than other biomarkers and becomes elevated relatively early in the disease process. While contemporary cardiac troponin may not be elevated within the first 2 to 4 hours after symptom onset, newer high sensitivity troponin assays have detectable elevations much earlier. It is also true that the amount of troponin released, and therefore the time to elevation, is proportional with infarct size, so it is unlikely to have a negative initial troponin with larger infarcts. Regardless of infarct size, most patients with true ischemia will have elevations in troponin within 6 hours, and negative troponins at this point effectively rule out infarct in most patients. Most assays use a cutoff value of greater than a 99th percentile as a positive test. In older, contemporary troponin assays, no detectable troponin is reported in most healthy individuals without the disease. Newer high sensitivity troponin assays often will report a normal detectable range in healthy individuals without the disease.

Several tools and scores have been developed to assist in the workup of ACS. These tools must be used with caution and in the appropriate context as none have been definitively shown to be superior to clinician judgment. Some common tools available are the TIMI (Thrombolysis In Myocardial Infarction) risk score, the GRACE (Global Registry of Acute Coronary Events) risk score, the Sanchis score, the Vancouver rule, HEART (History, ECG, Age, Risk Factors, and Troponin) score, HEARTS3 score, and Hess prediction rule. The HEART score was specifically developed for emergency department patients and has gained popularity in this setting.

Diagnosis

NSTEMI is diagnosed in patients determined to have symptoms consistent with ACS and troponin elevation but without ECG changes consistent with STEMI. Unstable angina and NSTEMI differ primarily in the presence or absence of detectable troponin leak.

- Scars prevent the mechanical failure of your heart's pumping action, which keeps our blood moving around our body, and us alive. But scar cells (called cardiac fibroblasts) also have side effects as they can obstruct the electrical signals that control the coordination of this same pumping action by the heart.

Loss of contractile myocardial tissue by myocardial infarction would result in depressed cardiac output if compensatory mechanisms would not be operative. Frank-Straub-Starling-mechanism and increased heart rate and contractility due to sympathetic stimulation are unlikely to chronically compensate for cardiac dysfunction. Structural left ventricular dilatation may be compensatory, but results in increased wall stress and, ultimately, in progressive dilatation and heart failure. In patients with myocardial infarction, we have shown left-ventricular dilatation in dependence of infarct size and time after infarction. Dilatation is compensatory first and normalizes stroke volume. However, left ventricular dilatation progresses without further hemodynamic profit and, thus, may participate in development of heart failure.

- Aortic Valve Stenosis & Regurgitation. The aortic valve controls blood flow from the heart to the rest of the body. In aortic stenosis, the valve narrows, restricting blood flow from the heart. In aortic regurgitation, the valve opening does not close completely, causing blood to leak backward into the heart.