The term “arrhythmia” comes from the Greek a-, loss + rhythmos, rhythm = loss of rhythm. According to the simplest definition, cardiac arrhythmia is defined as any abnormal heart rate or rhythm; the definition encompasses categories like sinus node dysfunction, supraventricular tachyarrhythmias, atrial fibrillation (AF), heart block, ventricular tachycardia and ventricular fibrillation (VF). As will be addressed in our series, AF is the most common cardiac arrhythmia seen by the clinician and the major cause of embolic stroke; VF is the most severe cardiac rhythm disturbance and one of the most important immediate causes of sudden cardiac death. Indeed, a major goal of basic and translational research in cardiac electrophysiology is to decipher the mechanisms underlying AF and VF.
Awareness that the heartbeat can become irregular is not new. As nicely noted by R. Ducas in 2007, “For thousands of years the only window physicians had into the hearts of their patients was through palpation of a pulse. The ancient Egyptians, Chinese and Greeks are credited with measurement and characterization of peripheral pulses and their association with illness”. In the modern era, the ‘discovery’ of “reentrant arrhythmia” is attributed to AG Mayer, who in 1906 applied combinations of electrical pulses to the contractile bell of jellyfish Cassiopea xamachana, and also rings of muscle cut from the ventricles of turtles, to demonstrate that a wave could be induced to propagate in one direction in the ring and then continue to circulate indefinitely. These experiments were extended by George Mines and William Garrey who demonstrated similar effects in dog ventricular muscle. The studies of Rothberger and Winterberg in 1909, led to the idea that arrhythmias can be generated by single ectopic electrical foci. A transformative milestone in understanding cardiac electrophysiology and arrhythmias, was the invention of the ECG by Willem Einthoven (1860-1927), who in 1924 received the Nobel Prize in Physiology or Medicine "for the discovery of the mechanism of the electrocardiogram". Clearly, the ECG revolutionized many aspects of clinical medicine, and established the basis/foundation for investigating cardiac arrhythmias. Another revolution came more than 70 years later when in 1998 Michel Haïssaguerre and colleagues demonstrated that ablation of ectopic triggers at the pulmonary veins effectively terminated up to 90% of cases of paroxysmal AF, which became a milestone in the clinical treatment of paroxysmal AF. Since then, there has been enormous progress in developing new, highly sophisticated tools for mapping and ablation of atrial and ventricular arrhythmias.
However, extension of ablative therapy to the highly heterogeneous persistent AF population has been significantly less successful. In addition, despite more than 100 years of research and speculation, we are yet to fully understand arrhythmia mechanisms and learn how to treat arrhythmias effectively.
The series of papers to which you are kindly requested to contribute, will include diverse topics related to basic and translational studies on acquired and inherited arrhythmias, arrhythmia classifications, old and new anti-arrhythmic drugs, dynamics and mechanisms of arrhythmias, in vivo and in vitro models, as well as genetics and mechanistically based studies in human patients. Our hope is that this Research Topic written by a few opinion leaders will inspire other clinicians and scientists in further helping to define the precise cellular and molecular bases of acquired and inherited arrhythmogenic cardiac diseases toward improving therapy for the benefit of the patient.
The term “arrhythmia” comes from the Greek a-, loss + rhythmos, rhythm = loss of rhythm. According to the simplest definition, cardiac arrhythmia is defined as any abnormal heart rate or rhythm; the definition encompasses categories like sinus node dysfunction, supraventricular tachyarrhythmias, atrial fibrillation (AF), heart block, ventricular tachycardia and ventricular fibrillation (VF). As will be addressed in our series, AF is the most common cardiac arrhythmia seen by the clinician and the major cause of embolic stroke; VF is the most severe cardiac rhythm disturbance and one of the most important immediate causes of sudden cardiac death. Indeed, a major goal of basic and translational research in cardiac electrophysiology is to decipher the mechanisms underlying AF and VF.
Awareness that the heartbeat can become irregular is not new. As nicely noted by R. Ducas in 2007, “For thousands of years the only window physicians had into the hearts of their patients was through palpation of a pulse. The ancient Egyptians, Chinese and Greeks are credited with measurement and characterization of peripheral pulses and their association with illness”. In the modern era, the ‘discovery’ of “reentrant arrhythmia” is attributed to AG Mayer, who in 1906 applied combinations of electrical pulses to the contractile bell of jellyfish Cassiopea xamachana, and also rings of muscle cut from the ventricles of turtles, to demonstrate that a wave could be induced to propagate in one direction in the ring and then continue to circulate indefinitely. These experiments were extended by George Mines and William Garrey who demonstrated similar effects in dog ventricular muscle. The studies of Rothberger and Winterberg in 1909, led to the idea that arrhythmias can be generated by single ectopic electrical foci. A transformative milestone in understanding cardiac electrophysiology and arrhythmias, was the invention of the ECG by Willem Einthoven (1860-1927), who in 1924 received the Nobel Prize in Physiology or Medicine "for the discovery of the mechanism of the electrocardiogram". Clearly, the ECG revolutionized many aspects of clinical medicine, and established the basis/foundation for investigating cardiac arrhythmias. Another revolution came more than 70 years later when in 1998 Michel Haïssaguerre and colleagues demonstrated that ablation of ectopic triggers at the pulmonary veins effectively terminated up to 90% of cases of paroxysmal AF, which became a milestone in the clinical treatment of paroxysmal AF. Since then, there has been enormous progress in developing new, highly sophisticated tools for mapping and ablation of atrial and ventricular arrhythmias.
However, extension of ablative therapy to the highly heterogeneous persistent AF population has been significantly less successful. In addition, despite more than 100 years of research and speculation, we are yet to fully understand arrhythmia mechanisms and learn how to treat arrhythmias effectively.
The series of papers to which you are kindly requested to contribute, will include diverse topics related to basic and translational studies on acquired and inherited arrhythmias, arrhythmia classifications, old and new anti-arrhythmic drugs, dynamics and mechanisms of arrhythmias, in vivo and in vitro models, as well as genetics and mechanistically based studies in human patients. Our hope is that this Research Topic written by a few opinion leaders will inspire other clinicians and scientists in further helping to define the precise cellular and molecular bases of acquired and inherited arrhythmogenic cardiac diseases toward improving therapy for the benefit of the patient.