An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs – the classic signs are a large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III (S1Q3T3), which occurs in 12–50% of people with the diagnosis, yet also occurs in 12% without the diagnosis.This is occasionally present (occurring in up to 20% of people), but may also occur in other acute lung conditions, and, therefore, has limited diagnostic value. The most commonly seen signs in the ECG are sinus tachycardia, right axis deviation, and right bundle branch block. Sinus tachycardia, however, is still only found in 8–69% of people with PE.ECG findings associated with pulmonary emboli may suggest worse prognosis since the six findings identified with RV strain on ECG (heart rate > 100 beats per minute, S1Q3T3, inverted T waves in leads V1-V4, ST elevation in aVR, complete right bundle branch block, and atrial fibrillation) are associated with increased risk of circulatory shock and death.Cases with inverted T in leads V1-3 are suspected with PE or inferior myocardial infarction. PE cases show inverted T waves in leads II and aVF, but inferior myocardial infarction cases do not show inverted T waves in II and aVF. Echocardiography
In massive and submassive PE, dysfunction of the right side of the heart may be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the right ventricle, a low-pressure pump, is unable to match the pressure.
Mitochondrial myopathies are types of myopathies associated with mitochondrial disease. On biopsy, the muscle tissue of patients with these diseases usually demonstrate "ragged red" muscle fibers. These ragged-red fibers contain mild accumulations of glycogen and neutral lipids, and may show an increased reactivity for succinate dehydrogenase and a decreased reactivity for cytochrome c oxidase. Inheritance was believed to be maternal (non-Mendelian extranuclear). It is now known that certain nuclear DNA deletions can also cause mitochondrial myopathy such as the OPA1 gene deletion. There are several subcategories of mitochondrial myopathies. Signs and symptoms
Signs and symptoms include (for each of the following causes):

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like syndrome (MELAS)
Varying degrees of cognitive impairment and dementia
Lactic acidosis
Strokes
Transient ischemic attacks
Hearing loss
Weight loss
Myoclonic epilepsy and ragged-red fibers (MERRF)
Progressive myoclonic epilepsy
Clumps of diseased mitochondria accumulate in muscle fibers and appear as "ragged-red fibers" when muscle is stained with modified Gömöri trichrome stain
Short stature
Kearns–Sayre syndrome (KSS)
External ophthalmoplegia
Cardiac conduction defects
Sensorineural hearing loss
Chronic progressive external ophthalmoplegia (CPEO)
Progressive ophthalmoparesis
Symptomatic overlap with other mitochondrial myopathies

Cause
Zidovudine, an HIV medication can cause red ragged fiber myopathy. Diagnosis
Muscle biopsy: ragged red fibers in Gömöri trichrome stain. Treatment
Although no cure currently exists, there is hope in treatment for this class of hereditary diseases with the use of an embryonic mitochondrial transplant. References


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