Inappropriate sinus tachycardia is an uncommon and poorly understood syndrome that is defined by non-paroxysmal elevated resting heart rates greater than 100 bpm and/or an exaggerated heart rate response to exercise or stress [57, 58]. The majority of patients with IST are women with the literature citing as many as 90 % of patients [59, 60]. Symptoms include palpitations, weakness, fatigue, lightheadedness, and near syncope. The diagnosis is made when ambulatory monitoring shows elevated resting heart rates (i.e. average heart rate >90 bpm) on a 24-h Holter monitor. It is important to exclude secondary causes of sinus tachycardia, such as drugs, hyperthyroidism, fever, anemia, and infection. There is overlap between the diagnosis of postural orthostatic tachycardia syndrome (POTS) and IST. POTS is defined as the presence of symptoms due to orthostatic intolerance with a heart rate increase of ≥30 bpm (or heart rate that exceeds 120 bpm) within the first 10 min of standing or upright tilt that is not associated with a decline in blood pressure or any debilitating conditions or medications that would diminish vascular tone [61]. POTS can be distinguished from IST by noting an abnormal increase in heart rate that is associated with changes in body position [62] and can be diagnosed using Tilt Table Testing [63]. No proven effective treatment exists for IST. Symptomatic patients can be treated with beta blockers as first line therapy along with lifestyle changes to eliminate any known triggers such as stimulants (caffeine, alcohol, medications). As anxiety can often be superimposed on IST management of anxiety with counseling and benzodiazepines may sometimes be required.

Ivabradine, a specific funny current (I_f) blocker, is currently under investigation as a promising new treatment option for IST. In the first randomized, double-blind placebo controlled crossover trial in patients with IST, Ivabradine significantly reduced heart rates and eliminated >70 % of symptoms reported at baseline; with 50 % of patients reporting complete symptom resolution [64]. In another study of 20 patients, comparing metoprolol succinate and Ivabradine, both drugs were shown to have similar effects on heart rate, however, Ivabradine was more effective than metoprolol in treating symptoms of IST with 70 % of patients reporting elimination of symptoms [65]. Ivabradine is currently not available in the United States and should be avoided in hypotensive, pregnant, and breastfeeding patients [62]. Radiofrequency ablation is rarely effective for IST and should only be considered in extreme symptomatic cases when medical treatment has failed and symptoms have clearly been shown to be associated with fast heart rates [66, 67]. IST is not usually associated with any structural heart disease or secondary causes of sinus tachycardia and tends to have a benign natural history [68].

Atrioventricular Node Reentrant Tachycardia (AVNRT) is the most prevalent paroxysmal supraventricular tachycardia (SVT) in females with a 2:1 predominance over males [69–73]. The diagnosis and management of AVNRT should not be any different from men.

Common signs and symptoms include the abrupt onset of rapid regular palpitations that can be associated with chest tightness, dizziness, and neck pulsations. Heart rates range from 140 to 250 in this rhythm and AVNRT is not typically associated with structural heart disease. Medications have only a modest effect in reducing the frequency of both AVNRT and AVRT. The 2003 ACC/AHA guidelines recommend catheter ablation as first line treatment (Class I) for patients with recurrent symptomatic episodes, patients with infrequent or single episodes who desire definitive treatment, and for patients with infrequent, well-tolerated AVNRT [74].

In those patients who prefer medical management over ablation, standard medical therapy includes non-dihydropyridine calcium channel blockers, beta blockers, or digoxin as first line therapy. Patients should be taught to perform vagal maneuvers (deep cough, bearing down, squatting) immediately at the onset of symptoms as this has greater efficacy than medical therapy. The 30-day recurrence rate following treatment with diltiazem [75] was 60 and 20–40 % with flecainide [76]. The decision to medically manage or ablate should be patient specific and should take into account frequency and duration of symptoms, the effectiveness and tolerance to drugs, and presence of structural heart disease. Radiofrequency ablation is recommended in women who plan to become pregnant in the future to eliminate the possibility of AVNRT complicating the pregnancy. Ablation has a 96 % success rate with recurrence occurring approximately 3–7 %. Patients considering ablation must consider the risk of AV block and need for pacemaker implantation, which can occur in 2–5 % of cases. There is no gender difference in success rates, complications, or recurrence of AVNRT after ablation. However, it has been shown that physicians tend to take a more conservative approach with women; referring women later for ablation after trying more anti-arrhythmic therapy [77, 78].

AVRT is the second most common paroxysmal SVT in women and is twice as frequent in men. AVRT involves an extranodal accessory pathway that provides a second electrical connection (e.g. in addition to the AV node) between the atria to the ventricles. There are two types of pathways: (a) manifest pathways which conduct electrical signals back and forth between the atrium and ventricle and (b) concealed pathways which can only conduct electrical signals backward from the ventricle to the atrium. Only patients with manifest accessory pathways will have pre-excitation (i.e. delta waves) visible on the surface ECG and represent those patients who are potentially at risk for sudden death.

Delta waves are present on the ECG in 0.15–0.25 % of the general population. Wolf Parkinson White syndrome (WPW) is used to define patients with delta waves on the ECG and symptoms of tachycardia. WPW syndrome is more common in men, and men are more likely to experience atrial fibrillation [70]. The most important consideration in patients with pre-excitation on the ECG is risk stratification for sudden death. Sudden death can occur in the presence of atrial fibrillation/flutter when atrial signals are conducted 1:1 (i.e. at rates ≥200 bpm) to the ventricles over the accessory pathway. Therefore, all patients with delta waves present on the surface ECG must be referred for risk stratification. The clinical features of AVRT are similar to AVNRT and can be distinguished by a thorough electrophysiological study. Like AVNRT, medical therapy tends to be less effective at treating arrhythmias associated with accessory pathways. Drugs used to treat AVRT include, Class I agents such as procainamide, disopyramide, propafenone, and flecainide and Class III agents such as ibutilide, sotalol, and amiodarone. Catheter ablation should be performed for high risk patients, and considered in patients who are symptomatic or fail medical therapy. Outcomes are similar regardless of sex. Because of the increased incidence of SVT in women with accessory pathways during pregnancy, radiofrequency ablation should be considered before these patients attempt pregnancy [77].

Atrial fibrillation is the most common arrhythmia in the United States, affecting over three million people, and the incidence increases with age. It is a supraventricular rhythm with uncoordinated atrial activity demonstrated by fibrillatory (f) waves, with irregular, rapid ventricular response on ECG. Atrial fibrillation is more common in men, however, women tend to have more symptoms that last longer, occur more frequently, and have higher ventricular rates [79, 80]. In addition, women tend to have more impaired quality of life measures than men [81, 82].

Common symptoms include palpitations, fatigue, dyspnea, and dizziness. Physical exam may reveal an irregular pulse, irregular jugular venous pulsations, and variable loudness of first heart sound. Examination should entail seeking for evidence of valvular heart disease, heart failure, sleep apnea or thyroid disorders. Diagnosis is made by documentation on ECG, 24-h Holter or event monitoring.

Management of patients with atrial fibrillation involves the decision to restore and maintain sinus rhythm (i.e. rhythm-control algorithm) versus heart rate control (i.e. rate-control algorithm). Rate control of atrial fibrillation can be achieved with a combination of beta blockers, calcium channel blockers, or digoxin. Restoration of sinus rhythm can be achieved either through electrical cardioversion or pharmacologic cardioversion and sinus rhythm can be maintained with antiarrhythmic medications.

Women tend to fare worse than men with medications for management of atrial fibrillation. Rate-control algorithms are associated with an increased risk of bradycardia, while subgroup analysis of the RACE study (Rate Control versus electrical Cardioversion study) [83] found that women randomized to rhythm-control algorithms did far worse than women managed according to rate-control. Women randomized to rhythm-control were three-times more likely to die from cardiovascular causes, and five-times more likely to develop heart failure or thromboembolic complications than women in the rate-control arm. Similar trends were not observed in men when comparing randomization strategies. Women also experience markedly elevated rates of medication-induced prolonged QT syndrome and torsades de pointes when taking any class of antiarrhythmic medication compared to men. Thus, these factors should be taken into consideration when deciding upon a rhythm-control algorithm with women.

Perhaps as a consequence of the adverse outcomes associated with antiarrhythmic therapy, women are less often treated according to a rhythm-control algorithm and are referred less frequently for cardioversion despite having worse symptoms and longer duration of symptoms than men. Women are also referred less often or later than men for radiofrequency ablation of atrial fibrillation despite similar success rates [84, 85]. Radiofrequency catheter ablation of atrial fibrillation is considered in highly symptomatic patients when symptoms are refractory to medical therapy.

Women have higher rates of thromboembolic complications compared to men, especially those over the age of 75. Elderly women are at especially high risk for disabling strokes, however, despite this finding, are less likely to be started on warfarin [86, 87]. Importantly, anticoagulation should be considered in all women with a CHA2DS2-Vasc score ≥2 who do not have any contraindication to anticoagulation.

Associated with atrial fibrillation is atrial flutter, a more organized rhythm with saw-tooth pattern of regular activation called flutter waves (f waves), visible in lead II, III, AVF. In atrial flutter, atrial rates range from 240 to 320 bpm, with inverted flutter waves in the inferior leads (II, III, AVF) and upright flutter waves in V1. Two-to-one AV block is common and can lead to atrial rate of 120–160. Medical therapy of atrial flutter is similar to atrial fibrillation. Because medications tend to be ineffective in atrial flutter, the ACC/AHA guidelines consider catheter ablation to be first line therapy for recurrent atrial flutter regardless of symptoms and cardioversion as first line treatment for the first episode of atrial flutter [74]. Radiofrequency ablation of typical atrial flutter has a 95 % efficacy rate with low procedure-related complication rates.

Atrial fibrillation and atrial flutter are frequently observed together. Following flutter ablation, the incidence of atrial fibrillation is dependent on whether atrial fibrillation was present prior to flutter ablation. For those patients with mostly atrial fibrillation prior to flutter ablation 86 % will develop persistent atrial fibrillation; while 8 % develop atrial fibrillation following flutter ablation when it had not been documented previously.

Gender differences in atrial tachycardia have not been as well studied [88]. Rates appear to be similar between men and women with similar outcomes following radiofrequency ablation [88, 89]. Focal atrial tachycardia occurs when an electrical impulse eminate from a site outside of the sinus node. It tends to occur in older patients with structural heart disease or underlying medical and pulmonary conditions. The ECG reveals a non-sinus P wave morphology and axis, and a narrow QRS complex. Although there are no large studies assessing the efficacy of different pharmacological strategies, medications such as beta-blockers or calcium channel blockers are typically the first line of medical therapy. Antiarrhythmic medications (typically class Ia or Ic) can be tried if beta-blockers or calcium channel blockers fail. An EP study should be pursued in cases of incessant atrial tachycardia or if symptoms continue despite medical therapy in paroxysmal atrial tachycardia. However, these procedures can be challenging since atrial tachycardia needs to be observed during the EP study to hone in on the focal site. The sedative medications used to make patients comfortable for the procedure tends to suppress atrial tachycardia.

Sex hormones also influence predisposition to ventricular arrhythmias. One study, demonstrated that postmenopausal women with idiopathic outflow ventricular tachycardia had decreased levels of estradiol compared to control postmenopausal women [90]. Postmenopausal women with idiopathic outflow ventricular tachycardia had a higher arrhythmia burden than controls, which was significantly reduced after 3 months of estrogen replacement therapy. Right ventricular outflow tachycardia, which typically occurs in younger patients and in the absence of structural heart disease, also has gender specific triggers commonly occurring in women during the premenstrual state (i.e. luteal phase) and in men during states of stress and increased exercise [91].

The clinical presentation of ventricular tachycardia (VT) is variable based on underlying structural heart disease, comorbidities, and rate of the tachycardia. Patients can be asymptomatic or present with syncope or sudden cardiac death (SCD). Diagnosis is made by reviewing the ECG. VT needs to be distinguished from SVT with aberrant conduction, bundle branch block, or changes in QRS morphology due to metabolic abnormalities. Management of patients depends primarily on the clinical scenario. Unstable patients should undergo rapid direct current (DC) cardioversion; whereas hemodynamically stable patients can initially be managed with intravenous antiarrhythmics including amiodarone, lidocaine, procainamide and beta blockers. It is important to treat any medical conditions or electrolyte abnormalities, or remove any offending drugs or substances that may be contributing to VT. Antiarrhythmics in general have an uncertain role in the prevention of VT.

In the Framingham Study, significant sex-related differences in ventricular tachycardia and sudden cardiac death were found. Women tended to have SCD at an older age than men, usually lagging behind by 10 years, and less coronary heart disease [92, 93]. In addition, women had a lower incidence of SCD, one third of that in men [94]. While women are more likely to present with SCD at an older age they are also more likely than men to have return to spontaneous circulation [95].

Sex differences also exist in the risk factors and etiology of SCD in women. Causes beyond coronary artery disease need to be considered particularly in younger women, such as nonischemic cardiomyopathy, valvular heart disease, hereditary arrhythmias such as Long QT syndrome or congenital heart disease [96]. Thus, classic risk factors for coronary artery disease and ventricular tachycardia that are predictive of events in men may not apply as well to women, making the risk stratification of SCD in women more difficult. Bertoia et al., identified gender specific independent risk factors for SCD in 161,808 women enrolled in the Women’s Health Initiative Trial, which included African-American race, increased heart rate, higher hip to waist ratio, elevated white blood cell count, and heart failure [97].

Implantable cardioverter defibrillators (ICD) have been shown to decrease mortality when used for both primary and secondary prevention of sudden cardiac death in both men and women. There are some contradictions regarding the mortality outcomes between genders. The Antiarrhythmics Versus Implantable Debfibrillators Trial (AVID) investigators showed no gender difference between men and women with ICD for the secondary prevention of SCD [98]. However, the Sudden Cardiac Death in Heart Failure trial (SCD-HeFT) study found statistically significant decrease in mortality in men who received ICDs but not in women, likely because it was underpowered to detect a difference due to low enrollment of women [99].

A review of the Medicare registry from 1991 to 2005 of a large cohort of subjects diagnosed with ischemic heart disease revealed a two- to threefold increased risk of appropriate ICD therapies for VT/VF at 1 year in men versus women who underwent ICD implantation for either primary or secondary prevention [100]. Importantly, however, subgroup analysis of MADIT II [101] and DEFINITE trial [102] found no difference in ICD effectiveness in patients with either ischemic or nonischemic cardiomyopathy based on gender.

Women are less likely than men to be referred for ICD implantation for both primary and secondary prevention of SCD, with women being 61 % less likely than men to receive an ICD [103, 104]. Reasons for this disparity are unknown [105, 106]. However, it is important to recognize that based on the currently available data ICDs appear to be equally effective at reducing mortality in women and men.

As mentioned earlier, gender differences do exist regarding acquired and inherited long QT syndrome (LQTS), as well as the risk for TdP leading to SCD. Women have increased prevalence of both drug induced and inherited LQTS that appear to correlate with variations in sex hormone levels. Women with prolonged QT intervals are more likely to have increased cardiac events during the post- partum period while men are more likely to suffer syncope and sudden death at a younger age prior to the onset of puberty [91, 107].

Congenital LQTS is characterized by prolonged QT intervals caused by gene mutations that encode sodium or potassium ion channels. Over 300 different LQTS-related mutations have been identified that affect five main genes (KVLQT1, HERG, SCN5A, KCNE1, and KCNE2) [108]. Three major subtypes (LQT1, LQT2, LQT3) comprise the majority of cases. The LQTS subtype can sometimes be inferred from the surface ECG: LQT1 is characterized by broad-based T waves and exercise induced arrhythmic events, LQT2 has low amplitude, notched T waves and auditory induced arrhythmias, and LQT3 has long isoelectric ST segment and SCD events during sleep. Patients are treated with beta blockers and those with high risk markers or with significant symptoms refractory to medications should be considered for ICD implantation. The risk for cardiac events have distinct age and gender predilections in congenital LQTS. Prior to adolescents, boys are at elevated risk for cardiac events. At adolescence, this risk reverses and girls maintain an increased risk of cardiac events into menopause [109].

Women are also more likely to develop drug-induced prolonged QT especially from antiarrhythmics that prolong ventricular repolarization and from electrolyte and metabolic abnormalities. Women are more likely to develop TdP from all classes of antiarrhythmic medications, including Vaughn William Class IA drugs such as quinidine and from Class III drugs such as sotalol [91]. Class IC drugs like flecainide do not increase QT interval. Primary practitioners need to be aware of different gender responses to drugs especially cardiovascular medications. Drug metabolism is affected by changes in hormone levels brought on by menopause, pregnancy and menstruation. Also, women have higher CYP3A4 activity than men which is known to metabolize more than 50 % of medications [110].

Arrhythmogenic Right Ventricular Dysplasia (ARVD) is an important cause of sudden cardiac death and has an autosomal mode of inheritance. This disorder is characterized by fibrofatty infiltration of the ventricles. Diagnosis is made by characteristic epsilon waves seen on ECG and evidence of fatty infiltration on gadolinium-enhanced MRI. Most case series reports ARVD as being more prevalent in men than women, however, there is no difference in the clinical presentation of ARVD between men and women [111].

Brugada is an autosomal dominant arryhythmogenic disorder of cardiac sodium channels caused by mutation in SCNA5 gene that predisposes patients to polymorphic ventricular tachycardia or ventricular fibrillation. It affects men more commonly than women, and men tend to have more syncope, aborted SCD, increased ventricular fibrillation inducibility, greater ST segment elevation, and greater rates of spontaneous type 1 ECG pattern [112]. Finding a type 1 ECG Brugada pattern is recognized as a risk factor for SCD. Women with Brugada syndrome who presented with resuscitated SCD or an appropriate ICD shock were less likely to have spontaneous type 1 ECG pattern when compared to men [113]. Although women appear to be at lower risk it is not clear whether our current risk factors are able to clearly identify women at high risk. High risk patients include patients with syncope, spontaneous type 1 ECG pattern, and those with a family history of SCD. These patients should be considered for cardiac defibrillator implantation.