A juvenile (estimated 3- to 6-month-old) female Scottish Fold cat was referred to cardiology specialists for evaluation of a murmur detected by a primary care veterinarian. The cat had been obtained several weeks earlier through a social media website and had an undisclosed medical history. The cat had blepharospasm caused by a suspected ocular viral infection and was being treated with topical ophthalmic erythromycin ointment and oral administration of lysine, but the owners reported no clinical signs of cardiac disease. On examination, the cat had a grade 5/6 left parasternal systolic murmur. Heart rate was 260 beats/min, and the rhythm was regular with moderately strong femoral pulses that were synchronous with the heartbeat. Echocardiography revealed mild left ventricular hypertrophy (left ventricular septal wall thickness, 6 mm [reference range,1 < 6 mm]; left ventricular free wall thickness, 7 mm [reference range,1 < 6 mm]) and a thickened and elongated anterior mitral valve leaflet. Systolic anterior motion of the mitral valve was evident, which caused mild mitral valve regurgitation and high left ventricular outflow tract velocity (5.3 m/s; reference range, 1.0 to 1.2 m/s)1 with a scimitar-shaped spectral Doppler ultrasound profile. Given the cat's young age and the echocardiographic characteristics of the mitral valve, a presumptive diagnosis of mitral valve dysplasia with severe outflow tract obstruction and secondary left ventricular hypertrophy was made, although a diagnosis of primary hypertrophic obstructive cardiomyopathy could not entirely be ruled out. On the basis of the cat's tachycardia and suspected J-point deviation noted on the echocardiographic timing lead, 6-lead ECG was performed (Figure 1).
A 6-lead ECG recording obtained from a juvenile Scottish Fold cat that was referred for evaluation of a heart murmur. Notice the sinus tachycardia with a mean heart rate of 230 beats/min. There is pronounced J-point elevation (0.2 mV). Paper speed = 50 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.534
A 6-lead ECG recording obtained from a juvenile Scottish Fold cat that was referred for evaluation of a heart murmur. Notice the sinus tachycardia with a mean heart rate of 230 beats/min. There is pronounced J-point elevation (0.2 mV). Paper speed = 50 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.534
A 6-lead ECG recording obtained from a juvenile Scottish Fold cat that was referred for evaluation of a heart murmur. Notice the sinus tachycardia with a mean heart rate of 230 beats/min. There is pronounced J-point elevation (0.2 mV). Paper speed = 50 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.534
ECG Interpretation
Electrocardiography revealed a sinus tachycardia (mean heart rate, 230 beats/min) with pronounced J-point elevation (0.2 mV). The J-point deviation was suspected to represent myocardial ischemia related to the severe outflow tract obstruction and tachycardia. Circulating cardiac troponin I concentration was not assessed. In attempts to blunt the tachycardia, reduce myocardial oxygen demand, and potentially reduce systolic anterior motion of the mitral valve and mitigate further development of left ventricular hypertrophy, the owners were instructed to treat the cat with metoprolol (12.5 mg) orally, once daily for 2 days, and then twice daily thereafter if the medication was well tolerated. At a follow-up evaluation 8 days after commencement of twice-daily dosing, the owners reported no change in the cat's clinical status. On examination of the cat, the murmur was persistent but subjectively softer (grade 3/6) and the heart rate was markedly reduced (130 to 150 beats/min), compared with the previous ECG findings, with a regular rhythm. Recheck ECG (Figure 2) revealed sinus bradycardia (mean heart rate, 136 beats/min) and suspected type II isorhythmic atrioventricular (AV) dissociation. The J-point deviation had resolved, suggesting resolution of myocardial ischemia. Echocardiography was not repeated at the follow-up evaluation but was scheduled to be performed 2 months later.
A recheck 6-lead ECG obtained from the same cat after 8 days of oral treatment with metoprolol (12.5 mg) twice daily. The mean heart rate is 136 beats/min. The J-point deviation has resolved. Notice the change in QRS complex morphology; complexes at the beginning and end of the recording are splintered in lead III, whereas other complexes (asterisks) are not. This likely represents type II isorhythmic atrioventricular dissociation with fusion junctional escape complexes secondary to sinus bradycardia. However, given the similar heart rate associated with each complex morphology, it is difficult to definitively determine which represent normal sinus complexes and which are escape complexes. The circle denotes a paper-fold artifact. Paper speed = 50 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.534
A recheck 6-lead ECG obtained from the same cat after 8 days of oral treatment with metoprolol (12.5 mg) twice daily. The mean heart rate is 136 beats/min. The J-point deviation has resolved. Notice the change in QRS complex morphology; complexes at the beginning and end of the recording are splintered in lead III, whereas other complexes (asterisks) are not. This likely represents type II isorhythmic atrioventricular dissociation with fusion junctional escape complexes secondary to sinus bradycardia. However, given the similar heart rate associated with each complex morphology, it is difficult to definitively determine which represent normal sinus complexes and which are escape complexes. The circle denotes a paper-fold artifact. Paper speed = 50 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.534
A recheck 6-lead ECG obtained from the same cat after 8 days of oral treatment with metoprolol (12.5 mg) twice daily. The mean heart rate is 136 beats/min. The J-point deviation has resolved. Notice the change in QRS complex morphology; complexes at the beginning and end of the recording are splintered in lead III, whereas other complexes (asterisks) are not. This likely represents type II isorhythmic atrioventricular dissociation with fusion junctional escape complexes secondary to sinus bradycardia. However, given the similar heart rate associated with each complex morphology, it is difficult to definitively determine which represent normal sinus complexes and which are escape complexes. The circle denotes a paper-fold artifact. Paper speed = 50 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 5; 10.2460/javma.255.5.534
Discussion
In ECG tracings, the ST segment (also known as the J point) represents the period during which the ventricular myocardium repolarizes; in normal myocardium, the ST segment should be isoelectric to the TP segment.2 The ST segment may appear elevated when regions of the ventricle remain depolarized at rest because of ischemia or injury and generate currents that travel away from the normal mean electrical axis after the remainder of the healthy ventricle has repolarized.3,4 As a result, the normally isoelectric baseline may move in a negative direction, creating a relative electrical shift that appears to be ST elevation (STE) but is actually TP-segment depression.4,5 In humans, STE is associated with transmural myocardial ischemia or infarction, acute pericarditis, hypertrophic cardiomyopathy with or without left ventricular outflow tract obstruction (LVOTO), Takotsubo (stress) cardiomyopathy, and Brugada patterns, but it has not been widely reported in the veterinary medical literature.3,4,6–10
Several proposed mechanisms have been implicated in STE associated with hypertrophic cardiomyopathy in humans, and each may apply to the cat of the present report.9,11,12 Hypertrophic cardiomyopathy can result in altered oxygen demand and delivery and in inefficient contractility and relaxation. Histologic postmortem studies13,14 of cats, dogs, and people with hypertrophic cardiomyopathy have revealed abnormal coronary vasculature, most commonly in the ventricular septum, with narrowed lumina and thickening of the tunicae media and intima. Additionally, high intracavitary forces generated by a hypertrophied left ventricle (particularly one affected by an outflow tract obstruction) may compress the microcirculation and cause the subendocardial layers to receive diminished blood flow.12 Wave-intensity analysis of hypertrophic hearts has revealed competing forward and backward flow forces in coronary blood flow, which lead to coronary flow reversal during systole and higher flow velocity during diastole.12 Mismatch of oxygen supply and demand may be exacerbated further in hypertrophied hearts with increased heart rate and LVOTO as a result of a prolonged ejection phase and a shortened diastolic phase.12 It is likely that the severe LVOTO and tachycardia in the cat of the present report were major causes of the J-point deviation, especially given the resolution of the J-point abnormalities after treatment with metoprolol.
β-Adrenoceptor blockers reduce heart rate and oxygen consumption, which can lead to redistribution of transmural myocardial blood flow and improved diastolic myocardial perfusion.15 In patients with hypertrophic cardiomyopathy and LVOTO, administration of β-adrenoceptor blockers reduces the outflow tract gradient.16 Negative chronotropy prolongs diastole and coronary perfusion time. Additionally, negative inotropy results in a reduction in the backward compression wave and prevents retrograde coronary flow.12 The absence of J-point deviation in the follow-up ECG recording of the cat in the present report after treatment with metoprolol supported a reduction in myocardial oxygen demand or improvement in myocardial oxygen supply (or both) via the aforementioned mechanisms. In addition to resolution of the J-point deviation, recheck ECG also revealed periodic AV dissociation. Atrioventricular dissociation may occur when the normal sinus pacemaker is slowed or when there is abnormal acceleration of a junctional or ventricular focus.17 Administration of metoprolol likely caused sufficient slowing of the normal sinus rhythm to allow a junctional escape rhythm to periodically dominate. Reducing the dosage of the β-adrenoceptor blocker was considered, but because the cat was clinically unaffected, treatment was continued as previously prescribed. The owners did not return the cat for follow-up examination, but they reported during a telephone conversation 2 months after the time of initial diagnosis that metoprolol was being administered to the cat as prescribed. The cat had no clinical signs of cardiac disease.
Acknowledgments
The authors declare that there were no conflicts of interest.
References
1. Boon JA. Appendix four. In: Boon JA, ed. Veterinary echocardiography. 2nd ed. Chichester, England: Wiley-Blackwell, 2011;575.
2. Wagner GS, Lim TH, Strauss DG, et al. Interpretation of the normal electrocardiogram. In: Wagner GS, Strauss DG, eds. Marriott's practical electrocardiography. 12th ed. Philadelphia: Lippincott, Williams & Wilkins, 2014;16.
3. Samson WE, Scher AM. Mechanism of S-T segment alteration during acute myocardial injury. Circ Res 1960;8:780–787.
4. Im M, Stern JA. ECG of the Month. J Am Vet Med Assoc 2016;248:497–500.
5. Hall JE. Electrocardiographic interpretation of cardiac muscle and coronary blood flow abnormalities: vectorial analysis. In: Guyton and Hall textbook of medical physiology. 13th ed. Philadelphia: Saunders, 2016;139–153.
6. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol 1992;20:1391–1396.
7. Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349:2128–2135.
8. Akashi YJ, Goldstein DS, Barbaro G, et al. Takotsubo cardiomyopathy: a new form of acute, reversible heart failure. Circulation 2008;118:2754–2762.
9. Maron MS, Olivotto I, Maron BJ, et al. The case for myocardial ischemia in hypertrophic cardiomyopathy. J Am Coll Cardiol 2009;54:866–875.
10. Block CL, Barr CA, Gelzer AR. ECG of the Month. J Am Vet Med Assoc 2018;252:1214–1216.
11. Camici PG, Olivotto I, Rimoldi OE. The coronary circulation and blood flow in left ventricular hypertrophy. J Mol Cell Cardiol 2012;52:857–864.
12. Raphael CE, Cooper R, Parker KH, et al. Mechanisms of myocardial ischemia in hypertrophic cardiomyopathy: insights from wave intensity analysis and magnetic resonance. J Am Coll Cardiol 2016;68:1651–1660.
13. Liu SK, Roberts WC, Maron BJ. Comparison of morphologic findings in spontaneously occurring hypertrophic cardiomyopathy in humans, cats and dogs. Am J Cardiol 1993;72:944–951.
14. Cesta MF, Baty CJ, Keene BW, et al. Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy. Vet Pathol 2005;42:458–467.
15. Opie LH, Gersh BJ. β-Blocking agents. In: Drugs for the heart. 8th ed. Philadelphia: Elsevier, 2013;1–37.
16. Thompson DS, Naqvi N, Juul SM, et al. Effects of propranolol on myocardial oxygen consumption, substrate extraction, and haemodynamics in hypertrophic obstructive cardiomyopathy. Br Heart J 1980;44:488–498.
17. Marriott HJL, Conover MB. The action potential. In: Advanced concepts in arrhythmias. 3rd ed. St Louis: Mosby, 1998;32–36, 47–49.
