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an electrocardiogram is done is a likely predictor for most car-
diac outcomes. Similarly, the finding of unanticipated sagittal
sinus thrombosis on a CT scan or MRI will likely predict serious
neurological sequelae, again because CT scans of the head are
ordered in a subset of patients at risk for neurological events. In
their study, however, the authors analyzed data from the Cardio-
vascular Health Study (5577 participants) for a median of 12 years
of the primary cohort, and the Atherosclerosis Risk in Communities
Study (15,792 participants) for a median of 22 years as their rep-
lication cohort. Thus, by design, ascertainment bias is essentially
excluded and gives us reason to seriously examine the impact of
their findings in terms of pathophysiology and population-wide
screening.
PACs and AF
Paroxysmal AF often has discreet triggers that may manifest as
single PACs, bigeminy, couplets, or paroxysmal monomorphic atrial
tachycardia in addition to recorded AF. From their study, we can-
not glean whether the associated AF in patients with recorded
single PACs is paroxysmal or persistent. Furthermore, the loca-
tion of origin of the PACs, coupling interval, and whether or not
the absence of PACs on multiple electrocardiograms predicts
freedom from AF are unknown. Given the very high likelihood of
recordable AF in closely monitored patients with increasing age,
a possibility that the patients in the cohort with PACs were other-
wise at no higher risk for AF such as age, metabolic syndrome,
sleep apnea, etc is unclear.
PVCs and Congestive Heart Failure
Frequent PVCs as a possible sole cause for cardiomyopathy is
now well-established. At the same time, ventricular dysfunction
from many causes may present as or have associated PVCs. This
chicken and egg conundrum between PVCs and cardiomyopa-
thy is often difficult to solve, especially when multifocal PVCs are
present and detected after a cardiomyopathy was established. The
present study suggests that the electrical manifestation of PVCs
may well precede mechanical dysfunction (heart failure) either as
an early marker or as a cause.
Single-Lead Continuous Monitoring
There has been a plethora of devices for home and continuous
nonobtrusive cardiac monitoring. These vary from single-lead
electrocardiograms, pulse recordings, heart rate variability from
either of the two above, and similar devices that are integrated into
clothing, wearable devices, etc. Premature beats do not require
a 12-lead electrocardiogram to record and could easily be done
from single-lead recordings, and, indeed, with fairly simple trans-
forms and algorithms looking at pulse rate variability to diagnose,
quantify, and monitor. In the context of this burgeoning group of
devices and related technologies, the present study is timely and
important to integrate in future algorithm development.
The Issue of Death
A very important and nonintuitive finding from this study is that
a single premature beat, atrial or ventricular, is a marker of and
associated with the subsequent increased likelihood of death.
We cannot glean from this study and report whether the likeli-
hood of death is directly related to AF or heart failure but likely
presume this pathophysiological link. The link between AF and
death has been elusive to establish when reduction of preventa-
ble stroke and associated comorbidity is considered, and, further,
the possible incremental risk of PVCs over ventricular dysfunc-
tion alone with regard to cardiovascular mortality has also been
challenging. The present study with further analysis and repro-
duction from other cohorts may give us the answers that, in turn,
will leave difficult to answer questions on how aggressively we
need to monitor and intervene to prevent death when single pre-
mature beats are found.
Conclusion
A contemporary international leader – a teetotaler –
was asked why he doesn’t drink alcohol. The question
was posed as to why a single drink, particularly in a
social context, could possibly be harmful. The leader
who had bad family experiences with addiction and
alcoholism replied, “You can’t have two drags without
first having one!” Although a single premature beat
may seem innocuous, the mechanisms that underlie
the possibility of creating a single beat, particularly
with a re-entrant mechanism, establishes the
potential for repetitive manifestations of this building
block producing both arrhythmia and mechanical
dysfunction.
Dr Asirvatham is Consultant, Division of
Cardiovascular Diseases and Internal
Medicine, Division of Pediatric
Cardiology, Professor of Medicine and
Pediatrics Mayo Clinic College of
Medicine, Program Director EP
Fellowship Program, Director of
Strategic Collaborations Center for Innovation, Mayo
Clinic, Rochester, Minnesota.
Dr Kella is from the Department of Cardiovascular
Diseases, Mayo Clinic, Rochester, Minnesota.
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VOL. 2 • NO. 2 • 2017