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...................................................................................................................................... tachycardia, with or without reduced LV ejection fraction, procainamide was associated with fewer major cardiac adverse events and a higher proportion of tachycardia termination within 40 min compared with amiodarone. In case the mechanism of the arrhythmia is not fully understood, the arrhythmia should be treated as VT. 10.2 Irregular tachycardias A wide QRS irregular tachycardia is usually a manifestation of AF. Rarely, polymorphic VT and, very rarely, monomorphic VT may also present as irregular tachycardias. Electrical cardioversion is the acute treatment of choice in irregular pre-excited tachycardias associated with haemodynamic instability. Specific therapy of pre-excited AF is discussed in section 11. If the rhythm is well tolerated with a narrow QRS-complex irregular tachycardia, this should be considered likely to be AF, and rate control with beta-blockers or calcium channel blockers, and elective chemical or electrical cardioversion once thromboprophylaxis is in place, may be appropriate.4 11 Specific types of supraventricular tachycardia 11.1 Atrial arrhythmias 11.1.1 Sinus tachycardia Sinus tachycardia is defined as a sinus rate >100 b.p.m. On the ECG, the P wave is positive in leads I, II, and aVF, and biphasic/negative in lead V1. 11.1.1.1 Physiological sinus tachycardia The determinants of physiological sinus tachycardia are, by definition, physiological (effort, stress, or pregnancy), and may also arise secondary to other medical conditions or drugs (Table 10). The 12 lead ECG shows P-wave morphology typical of normal sinus rhythm. Physiological sinus tachycardia is treated by identifying and eliminating the cause. 11.1.1.2 Inappropriate sinus tachycardia IST is defined as a fast sinus rhythm (>100 b.p.m.) at rest or minimal activity that is out of proportion with the level of physical, emotional, pathological, or pharmacological stress.139 The tachycardia tends to be persistent, and most of the affected patients are young and female, but this disorder is not limited to that population.140 The underlying mechanism of IST remains poorly understood and is likely to be multifactorial (e.g. dysautonomia, neurohormonal dysregulation, and intrinsic sinus node hyperactivity). Recently, a gain-of-function mutation of the pacemaker hyperpolarization-activated cyclic nucleotidegated 4 (HCN4) channel has been reported in a familial form of IST.141 There is also evolving evidence that immunoglobulin G antibeta receptor antibodies are found in IST.142 The prognosis of IST is generally considered benign140 and the arrhythmia has not been associated with tachycardia-induced cardiomyopathy. 11.1.1.2.1 Diagnosis. Patients with IST have a wide spectrum of clinical presentations ranging from usually asymptomatic or minimally symptomatic palpitations to dyspnoea, exercise intolerance, dizziness, and light-headedness. The diagnosis of IST is one of exclusion of POTS, sinus re-entrant tachycardia, or focal AT from the superior part of the crista terminalis or right superior PV. Characteristically, 24 h Holter monitoring demonstrates a mean heart rate >90 b.p.m. with an exaggerated heart rate response >100 b.p.m. during waking hours.140 Tolerance exercise testing might also be considered to document the exaggerated heart rate or blood pressure response to minimal exercise. An EPS is generally not required in making the diagnosis, and should not be routinely performed unless, rarely, sinus node re-entry is suspected. 11.1.1.2.2 Therapy. Reassurance and lifestyle interventions such as exercise training, volume expansion, and avoidance of cardiac stimulants should be tried before drug treatment (Figure 6).139,143,144 As the prognosis of IST is benign, treatment is aimed at symptom reduction and may not be necessary. Beta-blockers have been used in patients with IST for several years, but may be needed at doses high enough to cause intolerable side effects such as chronic fatigue. Nondihydropyridine calcium channel blockers may also be used, but at doses that may cause hypotension, and the evidence regarding these drugs is limited.139,145 Ivabradine, a selective blocker of the ‘pacemaker current’ (If) in sinoatrial myocytes that directly slow the heart rate, has been found to be safe and effective in several small trials.146150 However, blockade of the If may perturb the feedback loop underlying baroreceptor control of autonomic balance, thereby increasing sympathetic activity to the heart.151 If this effect occurred chronically at therapeutic dosages, it would be a matter of concern for its remodelling and pro-arrhythmic potential. Ivabradine should be preferably co-administered with a beta-blocker when possible; this combination may also be more beneficial than each drug alone for IST.152 Ivabradine should not be taken during pregnancy or Table 10 Causes of physiological sinus tachycardia Physiological causes Emotion, physical exercise, sexual intercourse, pain, pregnancy Pathological causes Anxiety, panic attack, anaemia, fever, dehydration, infection, malignancies, hyperthyroidism, hypoglycaemia, pheochromocytoma, Cushing’s disease, diabetes mellitus with evidence of autonomic dysfunction, pulmonary embolus, myocardial infarction, pericarditis, valve disease, congestive heart failure, shock Drugs Epinephrine, norepinephrine, dopamine, dobutamine, atropine, beta-2 adrenergic receptor agonists (salbutamol), methylxanthines, doxorubicin, daunorubicin, beta-blocker withdrawal Illicit drugs Amphetamines, cocaine, lysergic acid diethylamide, psilocybin, ecstasy, crack, cocaine Other Caffeine, alcohol Downloaded from academic.oup.com/eurheartj/article/41/5/655/5556821 by guest on 07 October 2026