Page 224 - Feline Cardiology

Chapter 18: Arrhythmias and Other Electrocardiographic Abnormalities 229

the ventricles. Thus, the SA node continues to depolarize For example, when a series of 103 healthy, privately
with perfect regularity despite the occurrence of a PVC. owned cats underwent cardiovascular evaluations, 10
The result is that if a PVC occurs with very little prema- (10%) had arrhythmias on ECG: 7 of the cats did not
turity, the pause that follows the PVC will be only slightly have evidence of cardiomyopathy on echocardiographic
longer than the normal interval between heartbeats. evaluation (4 PVCs, 2 preexcitation, 1 VT), whereas 3
Conversely, if a PVC occurs very prematurely, a com- had evidence of cardiomyopathy: either HCM (PVCs in
paratively long pause will be present until the next sinus both cats) or arrhythmogenic right ventricular cardio-
beat. The length of the pause following a PVC is directly myopathy (1 cat; VT) (Paige et al. 2009). A higher preva-
related to the degree of prematurity of the PVC because lence here than in previous reports could be explained
the SA node continues to depolarize unfazed during the by the inclusion of ECG abnormalities identified on
PVC. Thus, while the normal beat may be blocked in the routine ECG, echocardiography, or both; typically, an
AV node during the PVC because the ventricles are in echocardiogram affords a period of monitoring the
the process of depolarizing from the PVC, the rhythm cardiac rhythm that is several times longer than the 30
resumes with perfect regularity thereafter. The P-P inter- seconds to 3 minutes of a routine ECG, increasing the
val from the heartbeat preceding a PVC to the heartbeat likelihood of identifying arrhythmias that occur only
following a PVC, should be exactly 2 normal P-P inter- intermittently. In practical terms, therefore, the inciden-
vals. This phenomenon describes a compensatory pause, tal finding of PVCs may be indicative of underlying
wherein the pause that follows the PVC in some sense structural heart disease in some but not all cats, and Arrhythmias
“compensates” for the prematurity of the beat and allows diagnostic evaluation as described in the initial part of
the rhythm to return to its previous pattern. By contrast, this chapter is appropriate in all cases.
PACs, which originate in the atria and depolarize the SA Systemic alterations such as hypokalemia, hypoxemia
node, often produce a noncompensatory pause, because (classically from pulmonary edema, pleural effusion, or
the firing pattern of the SA node is reset. pulmonary thromboembolism), anemia, hyperthyroid-
PVCs occur in 78–90% of healthy cats, who experi- ism (Peterson et al. 1982; Moïse et al. 1986), or excess
ence 0–150 PVCs daily (typically <60/day) (Hanås et al. circulating catecholamine concentrations (fear, pain,
2009; Ware 1999). The PVCs are significantly greater in anxiety, anger) may increase the propensity to forming
number in healthy older adult cats than healthy young PVCs, and even when an irreversible structural cardiac
adult cats (Hanås et al. 2009; Ware 1999): in one study, lesion is present, these correctable factors may be partly
no cat age 1–6 years old experienced more than or mostly responsible for the cardiac arrhythmia. For
9 PVCs/24 h (2 cats: none) compared to all cats age 8–14 example, epinephrine is a documented trigger for ven-
years old experiencing at least 1 PVC daily and 40% of tricular arrhythmias in cats (Hikasa et al. 1996). These
cats having >35 PVCs/24 h (Ware 1999). contributing or complicating factors represent thera-
In dogs and humans, PVCs are associated with virtu- peutic opportunities that should be identified and
ally any disorder, either cardiac or extracardiac. While addressed when a diagnosis of PVCs is made in cats.
this can be true in cats, significantly more cats with The signalment of clinical feline patients with PVCs
PVCs have concurrent structural heart abnormalities reflects the signalment of clinical feline patients with the
compared to dogs. Arrhythmogenic right ventricular disorder underlying the arrhythmia. For example,
cardiomyopathy is increasingly recognized in cats, and hypertrophic cardiomyopathy (HCM) occurs dispro-
its hallmark is ventricular arrhythmia (Fox et al. 2000; portionately more often in male cats, and a higher inci-
Harvey et al. 2005). In another retrospective study, the dence of PVCs can be expected in male cats for this
vast majority (102/106, 96%) of cats with PVCs or ven- reason. An unpublished subsample of 23 consecutive
tricular tachycardia (VT) on baseline ECG had an echo- cases drawn from a retrospective study (Côté and Jaeger
cardiographic diagnosis of structural heart disease, 2008) reveals that cats with PVCs or VT had a 2 : 1 gender
consisting of left ventricular concentric hypertrophy distribution (15 males:8 females, all 23 neutered), a
(n = 66), restrictive or unclassified cardiomyopathy mean age of 11.05 ± 4.2 years (median: 10 years), and a
(n = 17), or dilated cardiomyopathy (n = 6). By con- breed distribution of 18 domestic shorthairs and 5
trast, a significantly smaller proportion of dogs (95/138; domestic longhairs. Outside the patient population, no
69%) with PVCs or VT seen at the same time at the same gender or breed predilection has been noted in healthy
institution had an abnormal echocardiogram, indicating cats with PVCs, although they do have more PVCs when
a significantly higher prevalence of structural heart they are older, as described above (Hanås et al. 2009;
disease in cats with ventricular arrhythmias compared Ware 1999). Overall, information regarding age, gender,
to dogs (p <0.001) (Côté and Jaeger 2008). These results and breed appears to be of minimal use in approaching
may not reflect the feline population at large, however. the feline patient that has PVCs, and the usefulness of