**5.1. Deterioration of cardiac disease**

RCT can cause acute exacerbation of pulmonary congestion and edema in dogs with CMVI. In particular, if the first‐order chordae attached to the septal leaflet is ruptured, the clinical signs tend to more rapidly aggravate from acute volume overload and fulminant pulmonary edema [68], although the RCT in different mitral leaflet may not cause significant clinical signs. In dogs with significant RCT, marked increase in LA and pulmonary venous pressures can lead to acute pulmonary edema, pulmonary artery hypertension, and right‐sided heart failure [22, 130]. Therefore, these dogs usually require intensive care to stabilize the condition along with the standard therapy for CMVI.

Right‐sided heart failure is common, especially in dogs with long‐standing history of CMVI. Right‐sided heart failure can be occurred by either/both concurrent chronic tricuspid insuf‐ ficiency from myxomatous degeneration and/or the PHT from LA volume and pressure overload. Dogs with marked PHT generally show marked exercise intolerance with signs of weakness or collapse. Signs related to right‐sided heart failure (e.g., ascites, pleural effusion, hepatic and splenic congestion, and distention of the jugular veins with abnormal pulsations) can be noticed in physical examination. The presence and degree of PHT can be accurately assessed by Doppler echocardiography. Oxygen supplementation and pulmonary arterial vasodilator (e.g., sildenafil) are helpful to lessen clinical signs in dogs [131, 132].

Tachyarrhythmias are more commonly occurred in dogs having an enlarged LA. Common tachyarrhythmias in dogs with CMVI are supraventricular premature beats, atrial fibrillation, and supraventricular tachycardia. If the tachyarrhythmia has ventricular rate >180 bpm, it can cause hemodynamically significant change in dogs with CMVI and cause an acute onset of pulmonary edema. This condition is more often seen in dogs with long‐standing CMVI. Therapeutic goals for these dogs are directed to relieve the pulmonary edema along with the reduction in heart rate to an acceptable rate for improving cardiac output.

Left atrial rupture and cardiac tamponade can be occurred by marked dilation of LA in dogs with CMVI, because the LA becomes thin walled and more vulnerable to increase in pressure. One study found that endocardial splitting is more common in dogs with long‐standing CMVI [133]. Long‐standing and marked LA volume and pressure overload can progress to rupture of the LA, subsequently with the acute onset of hemopericardium, cardiac tamponade, and sudden death. Acute development of ascites, collapse, or marked exercise intolerance can be signs for sudden development of LA rupture and cardiac tamponade. Echocardiography is necessary for confirming the presence of significant pericardial effusion. Although immedi‐ ate pericardiocentesis may be helpful to alleviate clinical signs, the prognosis is usually poor.
