Most have a narrow QRS complex, although, occasionally, electrical conduction abnormalities may produce a wide QRS complex that may mimic ventricular tachycardia (VT). In the clinical setting, the distinction between narrow and wide complex tachycardia (supraventricular vs. ventricular) is fundamental since they are treated differently. In addition, ventricular tachycardia can quickly degenerate into ventricular fibrillation and death and merits different consideration. In the less common situation in which a wide-complex tachycardia may be supraventricular, a number of algorithms have been devised to assist in distinguishing between them. In general, a history of structural heart disease markedly increases the likelihood that the tachycardia is ventricular in origin. Sinus tachycardia is physiologic when a reasonable stimulus, such as the catecholamine surge associated with fright, stress, or physical activity, provokes the tachycardia. It is identical to a normal sinus rhythm, except for its faster rate (>100 beats per minute in adults). However, sinus tachycardia is considered part of the diagnoses included in SVT by most sources. Sinoatrial node reentrant tachycardia (SANRT) is caused by a reentry circuit localised to the SA node, resulting in a P-wave of normal shape and size (morphology) that falls before a regular, narrow QRS complex. It cannot be distinguished electrocardiographically from sinus tachycardia unless the sudden onset is observed (or recorded on a continuous monitoring device). It may sometimes be distinguished by its prompt response to vagal maneuvers.
Furthermore, in participants with baseline plasma viral load of <100,000 and >100,000 copies/mL, dolutegravir + abacavir/lamivudine compared to efavirenz/emtricitabine/tenofovir showed a reduction to <50 copies/mL in 85% and 71% compared to 73% and 72%, respectively. Post-marketing experience
In addition to the adverse reactions reported in clinical trials, the following adverse reactions have been reported voluntarily from a population of unknown size. As such, it is not always possible to estimate frequency or establish a causal relationship to drug exposure.Abacavir and/or Lamivudine

Digestive System: stomatitis
Gastrointentional: pancreatitis
General: weakness
Blood and Lymphatic Systems: aplastic anemia, anemia, enlarged lymph nodes, enlarged spleen
Hypersensitivity: sensitization reactions (including anaphylaxis), urticaria
Metabolism and Nutrition Disorders: hyperprolactinemia
Musculoskeletal System: muscle weakness, CPK elevation, rhabdomyolysis
Nervous System: paresthesia, peripheral neuropathy, seizures
Respiratory System: abnormal breath sounds/wheezing
Skin: hair loss, erythema multiforme. Suspected Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) have been reported in participants receiving abacavir primarily in combination with medications that are known to be associated with SJS and TEN, respectively. Amyotrophic lateral sclerosis
The safety and tolerability of Triumeq was evaluated for amyotrophic lateral sclerosis (ALS) patients as part of the Lighthouse trial, an open-label, phase 2a study, conducted in Australia beginning in late 2016 over 24 weeks. The study premise was human endogenous retroviruses, specifically human endogenous retrovirus K (HERV-K) may be a trigger or cause of ALS. Research has linked HERV-K to ALS based on increased nonspecific reverse transcriptase activity in the cerebrospinal fluid and blood of ALS patients, as well as HERV-K being found in the motor neurons of ALS patients.