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Received: 15-Nov-2022, Manuscript No. JCMEDU-22-82705;
Editor assigned: 18-Nov-2022, Pre-QC No. JCMEDU-22-82705 (PQ);
Reviewed: 02-Dec-2022, QC No. JCMEDU-22-82705;
Revised: 09-Dec-2022, Manuscript No. JCMEDU-22-82705 (R);
Published: 16-Dec-2022
Description Pathophysiology
Tachycardiomyopathies (TCMPs) are an important The mechanisms of Tachycardiomyopathies are not fully
cause of left ventricular (LV) dysfunction that clinicians defined, but include subclinical ischemia, abnormalities
should recognize because they are potentially revers- in energy metabolism, redox stress, and calcium over-
ible and have a significant impact on morbidity and load [2]. In animal models of persistent high-frequency
prognosis. They are classically defined as reversible im- atrial or ventricular pacing, ventricular injury is also
pairment of ventricular function induced by persistent associated with changes in myocardial electrophysiolo-
arrhythmia. However, it is becoming increasingly clear gy, including action potential prolongation and sponta-
that they can be induced by atrial and ventricular ec- neous ventricular arrhythmias [3]. Persistent left bun-
topy promoting dyssynchrony, and indeed the term dle branch block leads to lateralization of gap junctions
“arrhythmia-induced cardiomyopathy” is emerging to promoting functional anisotropy and apoptosis [4].
describe this phenomenon. A more current proposed This can be reversed by left ventricular stimulation in
definition emphasizes the etiology: ‘Atrial and/or ven- HF models. These molecular and cellular changes lead
tricular dysfunction secondary to rapid and/or asyn- to abnormalities in ventricular geometry and negative
chronous/irregular myocardial contraction, partially ventricular patterning. It is this reversibility of ventric-
or completely reversed after treatment of the causative ular function in these disorders that can be corrected
arrhythmia’. There are two categories of this condition: by treating the primary tachycardia, which is why it is
the arrhythmia is the sole reason for the ventricular important to quickly identify and treat Tachycardiomy-
dysfunction (arrhythmia-induced) and another reason opathies [5].
is, where arrhythmia worsens the ventricular dysfunc- Diagnosis
tion and/or worsens heart failure (HF) in a patient with
existing heart disease (arrhythmia-mediated), exclusion An electrocardiogram (ECG) is used to classify the type
of underlying structural heart disease may be challeng- of tachycardia. Based on the QRS complex, they can be
ing because current imaging techniques such as MRI divided into narrow and wide complexes [6]. Equal to
cannot readily identify diffuse fibrosis, which itself may or less than 0.1 s for a narrow complex. They are listed
be primary or secondary to the effects of the arrhyth- in order from most common to least common:
mia promoting ventricular wall dyskinesia and valvular Narrow complex :
stretch or regurgitation [1].Tachycardia, also called tach- • Sinus tachycardia, which originates in the sinoatrial
yarrhythmia, is a heart rate that exceeds normal resting (SA) node, near the base of the superior vena cava
heart rate. In general, a resting heart rate above 100
beats per minute is accepted as tachycardia in adults. A • Atrial fibrillation
heart rate above the resting rate can be normal (such as • Atrial flutter
during exercise) or abnormal (such as electrical prob-
• AV nodal reentrant tachycardia
lems in the heart).
• Accessory pathway mediated tachycardia
References
[1] Rangaraj VR, Knutson KL. Association between
sleep deficiency and cardiometabolic disease:
implications for health disparities. Sleep Med.
2016;18:19-35.