The hypothesis testing of inappropriate fast, irregular, or asynchronous myocardial contraction provoking cardiomyopathy has been the primary focus of numerous research efforts, especially during the last few decades. Rapid ventricular rates resulting from supraventricular arrhythmias and atrial fibrillation (AF), irregularity of heart rhythm—basic element of AF—and asynchrony, as a consequence of right ventricular pacing, bundle branch block, or frequent premature ventricular complexes, have been established as primary causes of arrhythmia-induced cardiomyopathy. The main pathophysiological pathways involved have been clarified, including neurohumoral activation, energy stores depletion, and abnormalities in stress and strain. Unfortunately, from a clinical point of view, patients usually seek medical advice only when symptoms develop, while the causative arrhythmia may be present for months or years, resulting in myocardial remodelling, diastolic, and systolic dysfunction. In some cases, making a definite diagnosis may become a strenuous exercise for the treating physician, as the arrhythmia may not be present and, additionally, therapy must be applied for the diagnosis to be confirmed retrospectively. The diagnostic process is also hardened due to the fact that strict diagnosing criteria are still a matter of discrepancy. Therapy options include pharmaceutical agents trials, catheter-based therapies and, in the context of chronic ventricular pacing, resynchronization. For the majority of patients, partial or complete recovery is expected, although they have to be followed up thoroughly due to the risk of recurrence. Large, randomized controlled trials are more than necessary to optimize patients' stratification and therapeutic strategy choices.
Whenever a physician confronts patients with cardiomyopathies embracing impaired atrial and/or ventricular function and chronic or repetitive arrhythmias, he has to keep in mind that what he sees may not represent final diagnosis but the consequence of an underlying primary causative mechanism. Which one came first, cardiomyopathy or arrhythmia? Over the past decades, vast amount of evidence has shown that almost any form of sustained or repetitive type of supraventricular arrhythmias can provoke myocardial dysfunction. Recent research data have demonstrated that asynchronous myocardial contraction, e.g. frequent premature ventricular complexes (PVCs), bundle branch block, and ventricular pacing are also capable of inducing impairment of ventricular function. All the aforementioned factors may result in reduction of ventricular ejection fraction (EF), ventricular dilatation, and finally in congestive heart failure, through pathophysiological pathways which do not differ substantially from the established ones for dilated cardiomyopathy. Existing evidence, however, has demonstrated the potential reversibility of such forms of cardiomyopathy, partial or complete, if appropriate treatment schemes are implemented.
Definitions: need for an update
It needs to be accepted that the terminology used so far does not apply to the whole burden of tachycardia-induced cardiomyopathy (TIC) causes and phenotypes. The classic definition refers to a condition described as impairment of left ventricular (LV) function secondary to chronic uncontrolled tachycardia, which is partially or completely reversible after normalization of heart rate and/or rhythm irregularity.1 Contemporary data have broadened the latter definition to include dysfunction of either atria and/or ventricles resulting from high atrial or ventricular rates, under the condition that there is no underlying structural disease.2 Moreover, recent studies have demonstrated that asynchronous myocardial contraction, such as that resulting from PVCs or right apical ventricular pacing can lead to more or less reversible myocardial dilatation and symptoms of congestive heart failure.3,4 If one attempted to summarize the above under the term arrhythmia-induced cardiomyopathy (AIC), these forms of cardiomyopathy could be described as atrial and/or ventricular dysfunction secondary to rapid and/or asynchronous/irregular myocardial contraction, partially or completely reversible after treatment of the causative arrhythmia. In our opinion, it may not be preferred for such a definition to include only cases without primary structural disease, as patients with known ventricular dysfunction are also prone to the consequences of TIC.5 Fenelon et al.6 have divided TIC into two subgroups: (i) pure TIC, when chronic tachycardia insults normal myocardium, being the sole mechanism of deterioration and (ii) impure TIC, when the above criteria are not met.
Clinical presentation and causes
Prevalence, incidence, and causality frequencies of AIC are difficult to estimate due to the small number of published studies, with retrospective design and small numbers of patients included.
The typical clinical presentation is of a patient with signs and symptoms of congestive heart failure and dilated cardiomyopathy.2 The causative arrhythmia may not be present; therefore, the treating physician has to be extremely careful when taking diagnostic decisions. Furthermore, patients often present only after months to years of tachycardia, as symptoms become apparent, and are usually unable to give precise information on potential time of initiation of the arrhythmia. Of course, it is not an unusual scenario patients being diagnosed only by imaging modalities, without complaining of any symptoms. The essential ventricular heart rate above which TIC diagnosis is confirmed has not been established yet. However, it can be presumed that rates >100 min−1 can have deleterious consequences.7
Gossage et al. were the first to report a case of a man with dilated cardiomyopathy resulting from rapid atrial fibrillation (AF).8 Since then, numerous studies have demonstrated that almost any form of sustained supraventricular arrhythmia may result in AIC (Figure 1).9–14 Of notice, in patients with AF, not only rapid ventricular rates but also the irregularity of ventricular response further deteriorates myocardial function.15 In all, 25–50% of patients with LV dysfunction and AF demonstrate some degree of TIC.5,16
Whipple et al., in their pioneer study of an experimental model of TIC, were the first to demonstrate that rapid pacing, either atrial or ventricular, can induce impairment of atrial or ventricular function.13 The detrimental effects of right ventricular (RV) apical pacing have been attributed to the abnormal electrical and mechanical activation pattern of the ventricles.17 The presence of mechanical dyssynchrony after long-term RV apical pacing is associated with LV dilation and deterioration of LV systolic function.18 In the modern era of randomized trials regarding cardiac pacing, it has been shown that ventricular desynchronization as a result of ventricular pacing, even when atrioventricular synchronization is preserved, increases the risk of hospitalization due to heart failure.19 In DAVID trial, patients with a standard indication for a defibrillator implantation, but without an indication for anti-bradycardia pacing, were randomized to either physiologic pacing (DDDR mode, lower rate of 70 bpm) or ventricular backup pacing (VVIR mode, lower rate of 40 bpm). The primary outcome measure (freedom from death and absence of hospitalization for new or worsened heart failure) was lower in the VVIR-40 group than in the DDDR-70 group, related to a significantly higher percentage of ventricular paced beats in the DDDR-70 group at 3 months' follow-up.20
Frequent PVCs, with or without episodes of non-sustained ventricular tachycardia are a recently appreciated cause of reversible cardiomyopathy.21 Plenty of research work exists concerning the cutoff burden of PVCs necessary for triggering mechanisms of cardiomyopathy. Various cut-off limits of PVC burden have been proposed to distinguish patients with AIC from those with primary dilated cardiomyopathy.22,23 Additional characteristics, as longer PVC duration, presence of non-sustained VT, multiform PVCs, and RV PVCs might be associated with AIC.23 Sustained idiopathic ventricular tachyarrhythmias have been also considered as common AIC causes.24 Arrhythmia-induced cardiomyopathy causes of ventricular origin are summarized in Figure 1.
Existence of arrhythmia does not mandate development of AIC. Mechanisms and pathways responsible in individual patients are not fully understood. Stronger risk factors contributing to development and degree of myocardial dysfunction are type of arrhythmia, heart rate, duration of tachycardia, and existing heart disease. Other factors include age, drugs administered, and comorbidities.6,7 All of the above determine the time of onset, duration, and grade of resolution of AIC.
Rapid ventricular rates
Whipple's experimental animal model provided invaluable information on the effects of rapid atrial or ventricular pacing to the myocardium, where severe systolic and diastolic dysfunction were induced.14 In another experimental animal model, Zupan et al.25 demonstrated that ventricular dysfunction was initiated early after initiation of atrial or ventricular pacing, was more pronounced after ventricular pacing and was proved reversible after pacing cessation. In humans, similar effects of long-term pacing have been demonstrated.26
Gross alterations in myocardial structure and function, neurohumoral derangements, and changes in the microscopic level are summarized in Figure 2.7,25,27–35 Of possible primary mechanisms responsible for the observed gross and cellular changes, the proposed predominant ones are myocardial energy depletion and myocardial ischaemia. Depletion of energy stores, such as creatine, phosphocreatine, and adenosine triphosphate, has been demonstrated in models of persistent tachycardia, together with lower levels of Na–K-ATPase activity, potential consequences of enhanced activity of Krebs cycle enzymes, and mitochondrial injury.36–39 Furthermore, alterations in the myocardial capillary network, structural and functional, result in impairment of myocardial blood flow reserve and induce myocardial ischaemia.32 A form of myocardial hibernation may be the reason why such changes are partially or completely reversed after the cessation of the causative arrhythmia.2 Oxidative stress, finally, is another mechanism proposed contributing to myocardial injury through imbalance between pro-oxidant and anti-oxidant pathways and mitochondrial DNA damage.40
Asynchronous myocardial contraction, for example RV pacing or bundle branch block repeals normal ventricular activation through the His-Purkinje system. Beyond the altered electrical activation, the mechanical activation patterns changes simultaneously, resulting in redistribution of myocardial strain and work and subsequently less effective contraction.41 Adrenergic innervation of the left ventricle during chronic pacing from the apex of the right ventricle by I123-metaiodobenzylguanidine (MIBG) scintigraphy has been assessed. It has been demonstrated that the vast majority (89.7%) of paced patients had regional defects of I123-MIBG uptake, predominantly in the inferior (92.3%) and apical (38.5%) wall.42 Myocardial perfusion defects may be present in up to two-thirds of patients after long-term RV apical pacing.43 The distinct pathophysiological pathways involved in the PVC-induced cardiomyopathy remain unclear, although similar mechanisms as those in RV pacing are implicated. It has not been proved that the heart rate is in fact high, probably it does not differ between patients with and without cardiomyopathy.44 The number of PVCs, expressed as the percentage of PVCs to the total number of QRS complexes or as the PVC sum per day has been used as a criterion of PVC-induced cardiomyopathy, although trials comparing pathophysiological consequences among groups of patients with different PVC burden are lacking.22,44,45 Moreover, interpolated PVCs—total numbers and percentage of the whole number of PVCs—have been demonstrated to be independent determinants of PVC-induced cardiomyopathy.44
Asynchrony is also evident in the case of AF. The loss of atrial contraction results in a 15–20% reduction of cardiac output and alterations in LV filling times and properties, due to atrioventricular asynchrony. Mitral regurgitation is worsened and pulmonary wedge pressures are elevated.46 It has been proven that irregular sequence of RR intervals produces adverse haemodynamic consequences that are independent of heart rate.47 The Starling mechanism relating myoﬁbre length to the strength of ventricular contraction and the force–interval relation are two potential mechanisms connecting irregularity of RR intervals and reduced cardiac output.
Atrial remodelling as a phenomenon resulting from incessant tachycardia has been called atrial TIC.2 The mechanisms contributing to atrial remodelling–atrial dilatation and systolic dysfunction—differ substantially from those for ventricular myocardium. Alterations of calcium handling, driven from down-regulation or altered function of the L-type Ca(2+)-channel and an increased Ca(2+) extrusion via the Na(+)/Ca(2+)-exchanger have been proposed as primary ionic changes.48 Furthermore, in an animal model of experimental rapid ventricular pacing-induced congestive heart failure, tissue apoptosis, inflammatory cell infiltration, and cell death were demonstrated. Maximum changes in the left atrium occurred earlier and were larger than in left ventricle, along with faster mitogen-activated protein kinase activation and raised levels of transforming growth factor-β1 in the left atrium.49
Time progression and recovery
Early haemodynamic changes are evident almost immediately after initiation of rapid ventricular rates. In a dog model of heart failure, acute onset of pacing resulted in a decrease in arterial blood pressure and cardiac output and increases in right atrial and pulmonary wedge pressure in 24 h which persisted after 3 weeks of pacing.50 In most animal models, changes in LV filling and contraction properties have been completed by 4–5 weeks of rapid pacing.28,31 Furthermore, pressure–volume loops using intracardial recordings have been analysed before and immediately after short-term restoration of the normal ventricular activation sequence in chronic double-chamber paced patients—by switching from a DDD—to an AAI mode). End-systolic elastance and its ratio to effective arterial elastance were improved acutely after switching to AAI mode of pacing.51
Usually, patients seek medical advice only after months to years of symptomatic congestive heart failure. The time to recovery after treatment is considered to be rate- and duration dependent. During recovery, rapid clinical improvement has been demonstrated. In contrast, echocardiographic LV diastolic cavity size remains elevated with only a gradual and incomplete return towards normalization by 4 weeks of recovery.52 Nearly complete recovery of symptoms and LV contractility is expected within 3 months after rhythm or rate control of the tachyarrhythmia.53 Similar results were published in patients who underwent atrioventricular node ablation and pacemaker insertion due to AF with high ventricular rates despite optimal medical therapy.54 In contrast, Brignole et al. and the most recent randomized AIRCRAFT study did not confirm such significant differences in the New York Heart Association (NYHA) functional class or objective measures of cardiac function.55,56 Probably, concerns of the possible detrimental impact of RV apical pacing must be taken into account.
Two further points have to be taken into consideration. Left ventricular hypertrophy persisting after weeks of discontinuation of pacing may be attributed to post-pacing response of myocytes to hypertrophic triggers. This response may be further enhanced by persistent LV dilatation.27 More importantly, despite normalization of EF, persistent LV remodelling has been demonstrated (LV dimensions and volumes significantly and persistently elevated when compared with controls) with implications on duration and type of antiarrhythmic therapy.57
Diagnosis and proposed criteria
A definite diagnosis of AIC is often difficult to make. Most patients have some degree of atrial/ventricular systolic or diastolic dysfunction; however, the causative arrhythmia may or may not be present. Even if an arrhythmia is identified concomitantly with depressed myocardial function, the establishment of a cause–effect relationship is not always feasible. Consequently, a high index of suspicion is necessary. Because of the retrospective nature of diagnosis, the majority of physicians accept that once a theoretical possibility of dilated cardiomyopathy secondary to arrhythmia exists, it is of critical importance to apply antiarrhythmic therapy schemes early and wait for resolution of symptoms and partial or complete restoration of structural and functional properties of the myocardium. Criteria for TIC diagnosis have been proposed by Fenelon et al.: (i) dilatation of the heart or heart failure and (ii) chronic or very frequent cardiac arrhythmia (incessant supraventricular tachycardia, AF, or flutter, incessant ventricular tachycardia). Furthermore, they suggested that chronic tachycardia that occurs >10–15% of the day may result in cardiomyopathy and emphasized that TIC should also be suspected in patients with existing cardiomyopathy and coexisting arrthytmias.6
Efforts have been made to predict TIC by application of ventricular echocardiographic indexes. Fujino et al.9 concluded that LV size on admission was smaller for TIC patients (LV end-diastolic diameter 57.6 ± 7.2 mm, LV end-systolic diameter 49.4 ± 8.0 mm) than in the dilated cardiomyopathy group (LV end-diastolic diameter 63.4 ± 8.8 mm, LV end-systolic diameter 55.3 ± 9.6 mm, P< 0.05) and that TIC patients had better prognosis (cardiac death, heart failure hospitalization) during follow-up. In another study, an LV end-diastolic diameter ≤61 mm predicted TIC with a sensitivity of 100% and a specificity of 71.4%; in patients with EF≤30%, LV end-diastolic diameter of ≤66 mm predicted TIC with a sensitivity of 100% and a specificity of 83.4%. All patients with TIC showed improvement of EF≥15%, a finding not demonstrated in the dilated cardiomyopathy patients (ΔEF≥5%).53 Smaller enlargement of LV is thought to be caused by a relatively more rapid process, as TIC is, in contrast to the chronic degenerative process seen in the context of primary dilated cardiomyopathies.58
Level of asynchrony
Criteria of asynchrony level and type necessary for cardiomyopathy induction, as it appears during RV pacing, have not yet been established. It has been proved that LV dyssynchrony may be present in >50% of patients requiring permanent RV pacing and is associated with deterioration of LV systolic function and NYHA functional class.59 However, it is still under investigation if LV dyssynchrony appearing just after pacing initiation can indeed cause gradual LV functional deterioration and development of congestive heart failure.4
Burden of premature ventricular complexes
In the context of PVCs as a primary cause of cardiomyopathy, it has been shown that PVC-induced LV dysfunction is not limited to PVCs that arise in the right ventricle.22,60 Moreover, a certain PVC burden may facilitate diagnosis, discriminating patients with PVC-induced cardiomyopathy from those with arrhythmiogenesis secondary to cardiomyopathies. Different authors have concluded in different PVC burden cut-off limits. Baman et al. proposed a PVC burden of >24% as independently associated with PVC-induced cardiomyopathy (sensitivity 79%, specificity 78%). A lower cut-off point raised sensitivity to 90% but lowered specificity to 58%. The lowest PVC burden resulting in cardiomyopathy was 10%. A further criterion was an abnormal EF that improved by at least 15% or normalized (≥50%) after an effective ablation procedure (see the following treatment strategies section).22 Additional predictors of PVC-induced cardiomyopathy, beyond a proposed cut-off limit of ≥16% (sensitivity 100%, specificity 87%), were proposed by Hasdemir et al.24 These are male gender, absence of symptoms, persistence of PVCs throughout the day, and the presence of repetitive monomorphic PVCs. Another recent study from Munoz et al.23 concludes that a longer PVC duration, presence of non-sustained ventricular tachycardia, multiform PVCs, and RV PVCs may be associated with cardiomyopathy, the latter finding due to different PVC burden necessary for cardiomyopathy induction (burden ≥10% for RV originating PVCs vs. ≥20% for LV originating PVCs). Finally, efforts have been made to stratify patients according to cardiomyopathy risk related to the total number of daily PVCs. It has been concluded that if patients were divided into three groups (<1000/24 h, 1000–10 000/24 h, and >10 000/24 h), the prevalence of cardiomyopathy was 4, 12, and 34%, respectively.45
Recently, Bhushan and Asirvatham have proposed criteria regarding PVC-induced cardiomyopathy. They suggest that otherwise young healthy individuals, without abnormal cardiovascular substrate having over 20 000 PVCs per day, no more than two PVC morphologies, PVCs originating from outflow tracts or from the fascicles and with preserved myocardial wall thickness (no scars demonstrated to be echocardiography) are the best candidates for presumption of PVC-induced cardiomyopathy diagnosis.61
In the majority of cases, a definite diagnosis can be established only with the condition that elimination of the arrhythmia results in functional and structural improvement. In other words, treatment strategies have to be applied supposing the diagnosis, a hypothesis that may be confirmed retrospectively. Different kinds of therapy strategies are suitable for different arrhythmias, since the primary goal of therapy differs, targeting heart rate/rhythm or relief from ventricular asynchrony. Our therapeutic strategy consists of pharmacological regimens, catheter-based and device-based interventions.
Almost all categories of antiarrhythmics have been used in cases of arrhythmia-induced cardiomyopathies. β-blockers, digitalis, non-dihydropyridine calcium channel inhibitors, or combinations are widely used to achieve rate control in AF.62 Rate control strategy is considered to be non-inferior to rhythm control, provided that heart rate does not remain uncontrolled, except in severely symptomatic patients.63,64 If long-term ventricular rate control cannot be achieved, rhythm control strategies should be applied, including direct current cardioversion and Vaughan Williams Class Ic and III agents (see also catheter-based therapies).62 A variety of supraventricular arrhythmias can also be treated, at least initially, with antiarrhythmic agents, although, usually, in cases of induced cardiomyopathy, an ablation strategy might be the treatment of choice.53
When frequent PVCs are considered to be the primary cause, two alternative treatment strategies are feasible. The first would be the administration of antiarrhythmic agents, primarily amiodarone or, in the case of PVCs originating from the ventricular outflow tracts, non-dihydropyridine calcium channel inhibitor. The latter can be used provided that they do not deteriorate the patient's clinical status due to their negative inotropic effects. Amiodarone should be administered on a temporary basis only, as its toxic effects can occur unexpectedly. Its use has been proposed for 3–6 months in patients when there is uncertainty about final diagnosis, followed by focal PVC ablation as permanent treatment if PVCs are reduced and cardiac function recovers.61
However, we have to keep in mind that even though antiarrhythmic agents are capable of controlling the causative cardiomyopathy mechanism, the induced myocardial remodelling may be resistant to therapy. As described in previous paragraphs, Dandamudi et al.57 demonstrated the persistence of LV dilatation after TIC treatment. To confront with raised ventricular volumes, the long-term administration of β-blockers and angiotensin-converting enzyme inhibitors has been proposed.2,57,65
Numerous studies have manifested the dominant role of catheter-based interventions in the therapeutics of arrhythmias causing cardiomyopathy. Of importance, their rank in the therapeutic algorithm differs according to specific type of arrhythmia, myocardial dysfunction grade, and symptom severity. With ablation, abolition of the culprit arrhythmia is achieved in a significantly higher rate than with antiarrhythmic therapy, along with avoiding pharmacological agents, which, among others, pose the danger of proarrhythmic effects.
Ablation procedures are applicable for almost any type of supraventricular arrhythmias, such as atrial tachycardia, atrial flutter, atrioventricular nodal reentrant or atrioventricular reentrant tachycardias, with excellent results regarding symptoms relief and myocardial dysfunction reverse.10–13 As a significant clinical implication of ablation success, Pizzale et al.10 report that patients who fulfil the criteria for an implantable cardioverter-defibrillator (ICD) pre-ablation, may have such improvement of their ventricular function that they are not ICD candidates post-ablation.
Ablation strategies in AF are considered more complex. If poor response to pharmaceutical rate or rhythm control is the case or if left atrium ablation fails, atrioventricular node ablation can be performed, in order to improve symptoms and prognosis.62 Yet, whether ejection function may recover or deteriorate on a long-term basis due to permanent RV pacing remains an issue of controversy.54–56 Left atrium ablation is a well-documented procedure for elimination of paroxysmal and persistent AF, when trials of antiarrhythmics fail.62,66 Various authors have addressed the issue of AF ablation in patients with depressed LV function.67,68 Gentlesk et al. reported an improvement of EF of at least 5% in 82% of them, while the EF normalized in 72% post-ablation. Moreover, the success rate seems similar between groups of patients with normal and depressed ventricular function.68 On the other hand, while Lutomsky et al.69 confirmed the improvement of EF using cardiac magnetic resonance, they also reported a significantly reduced success rate of ablation procedure in patients with depressed ventricular function, imposing a multifuctorial mechanism responsible for baseline myocardial dysfunction.
Single or multiple PVC sites of origin can also be detected and eliminated by radiofrequency ablation after thorough activation-and/or pace mapping, when trials of antiarrhythmic agents fail.22–24,60 Success criteria differ. Baman et al.22 considered the ablation procedure effective if at least 80% of the PVC burden was abolished, while Munoz et al.23 have set a more strict criterion of complete elimination and induction inability of the clinical arrhythmia post-ablation. A follow-up period of at least 3–6 months post-ablation is necessary in order to access clinical status, myocardial function improvement (if present), and early detection of recurrence.
Modern dual-chamber pacing systems guarantee atrioventricular synchronization and incorporate sophisticated algorithms that minimize ventricular pacing, if not inevitable. A lot of research work exists on how the detrimental effects of chronic RV pacing could be prevented. Different pacing sites have been proposed, such as RV outflow tract, RV septum, and His region.70–72
In clinical practice, however, what has been widely proposed as the most reliable alternative is biventricular pacing. In patients with normal EF and conventional indication for pacemaker implantation, biventricular pacing may prevent the deleterious effects of RV pacing in myocardial function.73 Biventricular pacing in patients with ventricular dysfunction and an indication for permanent pacemaker (HOBIPACE study) also reduced LV end-diastolic and end-systolic volumes compared with patients who received conventional RV pacing. Left ventricular ejection fraction was higher in the biventricular pacing recipients.74 Furthermore, it has been reported recently that patients who were initially paced from RV and developed cardiomyopathy attributed to pacing, when received biventricular pacing, LV function, ventricular volumes, and symptoms were partially restored.75 Upgrade relieves symptoms, as well as exercise tolerance.75,76 Data have confirmed the effect of biventricular pacing in such patients in terms of ventricular dyssynchrony relief.76,77
Finally, cases of complete myocardial volume and systolic function restoration by biventricular pacing in patients with left bundle branch block and dilated non-ischaemic cardiomyopathy have been reported, highlighting the potential cause–effect relationship between intraventricular conduction disturbances and myocardial dysfunction.78
Follow-up and risk of recurrence
The optimal duration of follow-up has not been defined, although most patients seem to recover within 3–6 months.22,53 Serial echocardiographic studies and recordings for arrhythmia recurrence may be necessary. Although some degree of recovery is the rule, a form of irreversible cardiomyopathy should not always lead to exclusion of AIC diagnosis.
In case of recurrence, deterioration of myocardial function and severe symptoms has been reported, with the rate of deterioration being significantly faster than the initial episode. Additionally, if recurrence occurs, a relationship with sudden cardiac death has been described, but the possible pathophysiological pathways are not fully understood.79
Is there an answer to the riddle?
Reversible forms of cardiomyopathies due to arrhythmic causes represent an appreciable percentage of diagnoses in patients presenting with myocardial dysfunction and symptoms of congestive heart failure.80 However, even if the causative arrhythmia is apparent, the clarification of a cause–effect relationship sometimes provokes a diagnostic ‘headache’ for the treating physician, since diagnosis may be confirmed only retrospectively. Criteria proposed so far, especially in the context of frequent PVCs, vary substantially among researchers. In fact, larger registries and randomized trials are needed in order to diagnose and stratify patients more rationally, according to echocardiographic parameters and arrhythmic burden. Moreover, genetic variations making patients prone to such forms of cardiomyopathy should be traced. In conclusion, every individual patient must be investigated thoroughly and treated competently, as an automatic answer to such a dilemma should never been given.
Conflict of interest: none declared.