A diagnosis of inappropriate sinus tachycardia is primarily one of exclusion, and the following may be observed:
Exclusion of all other causes of sinus tachycardia
Common forms of supraventricular tachycardia (SVT) must be excluded
Normal P wave morphology
A resting sinus tachycardia is usually (but not always) present
Nocturnal dip in heart rate
Inappropriate heart rate response on exertion
Mean heart rate in 24hrs >95 bpm
Symptoms are documented to be due to tachycardia
Hypotension is occasionally observed
Syncope (fainting) is occasionally reported

Treatment
IST has been treated both pharmacologically and invasively, with varying degrees of success. IST, in and of itself, is not indicative of higher rates of mortality, and non-treatment is an option chosen by many if they have minimal symptoms.Some types of medication tried by cardiologists and other physicians include: beta blockers, selective sinus node If channel inhibitors (such as ivabradine), calcium channel blockers, and antiarrhythmic agents. Some SSRI drugs are also occasionally tried, as are treatments more commonly used to treat postural orthostatic tachycardia syndrome, such as fludrocortisone.Invasive treatments include forms of catheter ablation such as sinus node modification (selective ablation of the sinus node), complete sinus node ablation (with associated implantation of a permanent artificial pacemaker), and AV node ablation in very resistant cases (creation of iatrogenic complete heart block, necessitating implantation of a permanent artificial pacemaker). However, invasive treatments can also make the symptoms worse. See also
Supraventricular tachycardia
Sinus tachycardia
Postural orthostatic tachycardia syndrome
Dysautonomia

References
Further reading
Yusuf, Shamil; Camm, A. John (2005). "Deciphering the sinus tachycardias". Clinical Cardiology. 28 (6): 267–76. doi:10.1002/clc.4960280603. PMC 6654702. PMID 16028460. Still, A; Raatikainen, P;  et al. (2005).
Endometrial hyperplasia is a condition of excessive proliferation of the cells of the endometrium, or inner lining of the uterus. Most cases of endometrial hyperplasia result from high levels of estrogens, combined with insufficient levels of the progesterone-like hormones which ordinarily counteract estrogens proliferative effects on this tissue. This may occur in a number of settings, including obesity, polycystic ovary syndrome, estrogen producing tumours (e.g. granulosa cell tumour) and certain formulations of estrogen replacement therapy. Endometrial hyperplasia with atypia is a significant risk factor for the development or even co-existence of endometrial cancer, so careful monitoring and treatment of women with this disorder is essential. Classification
Like other hyperplastic disorders, endometrial hyperplasia initially represents a physiological response of endometrial tissue to the growth-promoting actions of estrogen. However, the gland-forming cells of a hyperplastic endometrium may also undergo changes over time which predispose them to cancerous transformation. Several histopathology subtypes of endometrial hyperplasia are recognisable to the pathologist, with different therapeutic and prognostic implications.The most commonly used classification system for endometrial hyperplasia is the World Health Organization (WHO) system, which previously had four categories: simple hyperplasia without atypia, complex hyperplasia without atypia, simple atypical hyperplasia and complex atypical hyperplasia. In 2014, the WHO updated the classification system and removed the distinction between simple or complex hyperplasia, instead only on presence or absence of atypia. Endometrial hyperplasia (simple or complex) - Irregularity and cystic expansion of glands (simple) or crowding and budding of glands (complex) without worrisome changes in the appearance of individual gland cells.