Electrocardiographic changes in small-Breed Dogs with Myxomatous Mitral Valve Disease (MMVD)

Introduction

Myxomatous mitral valve disease (MMVD), also known as chronic degenerative mitral valve disease, is the most common acquired cardiac disease in dogs, particularly affecting small-and toy-breed dogs. It is characterized by progressive nodular thickening and distortion of the mitral valve leaflets, resulting in mitral regurgitation. Chronic mitral regurgitation causes volume overload of the left atrium and left ventricle, leading to progressive cardiac remodeling characterized by myocardial stretch, chamber enlargement, and structural alterations. These changes may disrupt normal electrical impulse generation and conduction, predisposing affected dogs to conduction abnormalities and cardiac arrhythmias. Electrocardiographic manifestations of these alterations include P-mitrale (broad or notched P waves indicative of left atrial enlargement), tall R waves and widened QRS complexes suggestive of left ventricular enlargement, and various cardiac arrhythmias (Ogawa et al., 2022) [7] . Echocardiography remains the gold standard for the diagnosis and staging of MMVD. However, electrocardiography (ECG) serves as a valuable complementary diagnostic tool by detecting rhythm disturbances, conduction abnormalities, and electrical changes associated with cardiac remodeling. Although many ECG abnormalities may remain subtle or absent during the early stages of MMVD, progressive disease increases the risk of clinically significant arrhythmias that may manifest as syncope or, rarely, sudden cardiac death. Therefore, ECG provides important additional information for the comprehensive evaluation and clinical management of dogs with MMVD. The present study was undertaken to evaluate electrocardiographic parameters and rhythm abnormalities in 18 echocardiographic ally confirmed small-breed dogs with MMVD and to compare these findings with those of healthy control dogs.

Materials and Methods

Client owned dogs presented to small animal medicine ward, Veterinary clinical complex, College of Veterinary Science, Tirupati and Proddatur, with clinical signs of cough, dyspnea, exercise intolerance, syncope and abdominal distension were screened and echocardiographic ally confirmed for presence of MMVD. A total of 18 echocardiographic ally confirmed small-breed dogs with MMVD were subsequently subjected to electrocardiographic evaluation using a standard electrocardiograph (Aspen ECG-3 Plus) following the methodology described by Tilley (1992) [13] . Electrocardiograms were recorded at paper speeds of 25 and 50 mm/s with a standard calibration of 10 mm = 1 mV. The recordings were analysed for heart rate, rhythm, waveform amplitude, and interval durations in accordance with standard electrocardiographic guidelines (Willis et al., 2015) [14] .

Results

In the present study, Electrocardiographic parameters of 18 dogs with MMVD were compared with those of healthy control dogs. A non-significant increase in P-wave duration (0.05 ± 0.00 s) was observed in dogs with MMVD compared with healthy controls (0.04 ± 0.00s). No significant differences (p > 0.05) were detected in P-wave amplitude, QRS complex duration and amplitude, T-wave duration and amplitude, PR interval, QT interval, or ST segment between the two groups (Table 1). The predominant electrocardiographic abnormalities observed in dogs with MMVD were sinus tachycardia (12/18; 66.67%), P-mitrale (broad P waves) (10/18; 55.56%), ST-segment coving (5/18; 27.78%), notched P waves (4/18; 22.22%), low-voltage QRS complexes (3/18; 16.67%), P-pulmonale (3/18; 16.67%), and atrial fibrillation (1/18; 5.56%). Normal sinus rhythm was observed in 4 of 18 dogs (22.22%) despite echocardiographic evidence of MMVD (Table 2). P wave Duration (sec) 0.04±0.00 a 0.05±0.00 a Amplitude (mV) 0.43±0.22 a 0.25±0.05 a 2.

QRS complex Duration (sec) 0.03±0.00 a 0.04±0.01 a Amplitude (mV) 1.23±0.28 a 1.80±0.40 a 3.

T wave Duration (sec) 0.09±0.01 a 0.10±0.02 a Amplitude (mV) 0.26±0.10 a 0.30±0.10 a 4. PR interval(sec) 0.11±0.00 a 0.09±0.01 a 5. QT interval(sec) 0.13±0.02 a 0.16±0.02 a 6. ST segment(sec) 0.09±0.01 a 0.12±0.01 a Mean ± S.E followed by same superscript(s) do not differ significantly (p > 0.05)

Discussion

The electrocardiographic parameters of dogs affected with MMVD were within normal reference limits, except for a mild increase in P-wave duration (0.05 ± 0.00 s), which is suggestive of delayed intra-atrial conduction secondary to left atrial enlargement (P-mitrale). Although the increase was not statistically significant, Ogawa et al. (2022) [7] [2,4,5,6,8,9,10] . Normal sinus rhythm was also observed in a proportion of affected dogs, indicating that clinically important structural cardiac changes may occur despite minimal electrocardiographic abnormalities. Sinus tachycardia most likely reflected a compensatory response to reduced forward cardiac output and increased sympathetic activity rather than a primary arrhythmia (Tilley, 1992) [13] . P-mitrale and notched P waves were indicative of left atrial enlargement and altered atrial conduction associated with chronic volume overload (Santilli et al., 2018; Ogawa et al., 2022) [7] . P-pulmonale may indicate right atrial enlargement secondary to pulmonary hypertension in advanced MMVD. Low-voltage QRS complexes were probably associated with pleural or pericardial fluid accumulation accompanying congestive heart failure (Greeshma et al., 2023) [2] . ST-segment coving may reflect myocardial hypoxia, nonspecific electrolyte disturbances, or ventricular hypertrophy (Cote, 2010). The occurrence of atrial fibrillation was consistent with previous reports demonstrating that marked left atrial enlargement predisposes dogs to atrial fibrillation through atrial electrical remodelling and ectopic activity originating from the pulmonary veins (Chen et al., 2000; Rush, 2002; Guglielmini et al., 2020) [1,3,11] . During the 90-day treatment period, no significant changes were observed in routine ECG parameters within or between treatment groups. Nevertheless, dogs exhibiting sinus tachycardia, P-mitrale, notched P waves, and P-pulmonale showed progressive improvement in electrocardiographic findings following therapy. The dog diagnosed with atrial fibrillation received adjunctive antiarrhythmic therapy with oral diltiazem and digoxin in addition to standard cardiac treatment, resulting in restoration of normal sinus rhythm by the 90th day. These observations indicate that although routine ECG measurements remained largely unchanged, rhythm disturbances and conduction abnormalities improved with appropriate medical management.

Conclusion

This study demonstrates that electrocardiographic evaluation in small breed dogs with MMVD reveals a range of rhythm and morphological abnormalities that reflect the hemodynamic consequences of chronic mitral regurgitation. Sinus tachycardia and P-mitrale were the most frequent findings, reflecting sympathetic activation and left atrial enlargement, respectively. Although routine ECG parameters showed minimal change during therapy, electrocardiography proved valuable for detecting rhythm disturbances and monitoring their response to treatment. These findings support the use of ECG as a complementary diagnostic and monitoring tool alongside echocardiography in the clinical management of dogs with MMVD.

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