A Ventricular Septal Defect (VSD) is a congenital cardiac disease, causing communication between the left and right ventricle.
These can occur in numerous locations and the changes to be expected depends on the exact location.
The development of left-sided (most common in veterinary medicine) or right-sided congestive heart failure is possible.
Based on the precise findings, we will discuss appropriate management options. Some cases require monitoring, others medical management, and some surgical intervention.
Congenital Mitral Valve Dysplasia is a condition where the mitral valve (separating the left atrium and left ventricle) did not form correctly at birth. As a result, the valve does not close (coapt) normally.
This poor coaptation allows reverse blood flow (left ventricle into left atrium), which is termed regurgitation or insufficiency.
This disease is progressive in that the chambers will continue to dilate, but the valve structure likely will not change.
Routine rechecks are required to monitor for any changes to the left atrium or ventricle that may warrant additional testing or direct medical management of this disease.
Eventually, this disease can lead to the development of congestive heart failure (fluid in the lungs), which is a medical emergency that makes breathing very difficult.
Tricuspid Valve Dysplasia is a congenital disease where the tricuspid valve did not form properly in utero.
This condition allows tricuspid regurgitation (backwards blood flow) which causes a volume overload to the right heart.
The long-term prognosis is difficult to predict, but often favorable. Life-long medications and recheck appointments are often necessary.
Affected patients may eventually progress into right-sided congestive heart failure.
Clinical signs of right-sided congestive heart failure may include abdominal swelling (ascites) and/or pleural effusion (fluid inside the chest, around the lungs).
This may make breathing difficult and additional therapy will be required.
Pulmonic valvular stenosis is a congenital condition wherein the valve did not form properly in utero.
This valve does not open completely and makes the right ventricle work very hard to eject the blood volume.
Over time, this causes severe hypertrophy (thickening) of the right ventricle. Medications may help reduce this severe gradient. The recommended surgery for severe disease is a pulmonic
stenosis balloon valvuloplasty to open the abnormal valve.
This is an endovascular surgery, where a small incision is made over the jugular vein and the balloon is passed through the blood vessels to the pulmonic valve.
The goal of this procedure is to reduce the pressure gradient by 50% or more. As long as dogs are within the mild to moderate categories (less than 80mmHg), their quality of life and life expectancy is typically good to excellent.
Without surgery, patients with severe disease may eventually go into right sided congestive heart failure (fluid accumulation in the belly or thoracic cavity), develop life-threatening arrhythmias, or display weakness or collapse.
In some cases, the pulmonic valve annulus is also reduced (annular hypoplasia), which complicates or limits surgical options.
In severe cases, it may preclude a surgical option and we must manage these patients with medications alone.
In some breeds, an abnormal right coronary artery (R2A anomaly) can be present, which may make surgery difficult or potentially impossible.
An angiogram (contrast injected into the blood vessels) is necessary to investigate this prior to the valvuloplasty being performed.
Equivocal Subaortic Stenosis is a “grey zone” where we cannot tell if the patient has mild disease (affected) or no disease.
When patients are beyond one year of age, this is highly unlikely to progress or change.
Recheck echocardiograms beyond two years of age may be helpful to determine if there is progression, but often no follow up is required.
Subaortic Stenosis is a condition where the aortic outflow tract is narrowed.
Most frequently, this a result of a partially or fully encircling fibrous ring just below the aortic valve.
This can make it very difficult for blood to exit the left ventricle, causing marked elevation in left ventricular pressures.
In moderate to severe cases, this will then cause severe left ventricular hypertrophy (thickening). This disease is “fixed” (non-progressive) after 1 year of age.
Patients with this condition (even mild) are at increased risk for infective endocarditis (infection of the heart valves).
Any suspicion of infection (urinary tract, respiratory, tooth root abscess, skin infection, etc.) should be immediately diagnosed and treated based on the results of a culture and sensitivity profile. With severe disease, these
patients may develop ventricular arrhythmias and may have a higher incidence of sudden death.
Recheck physical examinations and electrocardiograms (ECGs) are recommended to monitor for any abnormal electrical activity that may require treatment.
A right to left Patent Ductus Arteriosus (Reversed PDA or rPDA) is a congenital defect where the ductus arteriosus (fetal vascular connection) remains present after birth.
The pulmonary pressures rise dramatically due to a problem within the lungs (Eisenmenger’s Physiology), causing blood to flow from the main pulmonary artery into the descending aorta.
This high concentration of deoxygenated blood causes a high degree of deoxygenated blood to flow to the back half of the body, particularly the kidneys.
This is seen clinically as differential cyanosis (blue/purple caudal membranes, pink cranial membranes). A rPDA results in severe elevations of the hematocrit (PCV or HCT) as the kidneys respond to the deoxygenated blood by signaling for more red blood cell production.
Affected patients will typically become neurologic (seizures, altered mentation, weakness, collapse, inappetance, or trembling) as the hematocrit rises.
These patients are also at risk for sudden death due to arrhythmias, neurologic conditions (embolic events or seizures), or potentially right-sided congestive heart failure.
There is no cure for this condition. Therapy is directed towards lowering the pulmonary pressures, thus reducing the degree of shunting and therapeutic phlebotomy (blood draws) as necessary to maintain the hematocrit around 60-65%.
The prognosis is typically poor; however, some patients will live for many years with optimal medical management.
A Patent Ductus Arteriosus (PDA) is a congenital defect where the ductus arteriosus (fetal vascular connection) remains patent after birth.
This allows blood to flow from the aorta into the main pulmonary artery.
If left untreated, this allows severe fluid overload to the left side of the heart. This causes severe left atrial and left ventricular dilation, eventually resulting in left-sided congestive heart failure (fluid on the lungs).
Affected patients will typically progress into congestive heart failure by 1 year of age and most patients will die by 3 years of age.
It is important to monitor these patients for the development of congestive heart failure as medications are required to control this condition and maximize life expectancy and quality of life.
Fortunately, with surgical correction, the life expectancy of patients with this condition is generally normal (unless advanced myocardial insult has happened before diagnosis).
The surgical procedure typically recommended is a transvenous occlusion, but the size of your pet may impact surgical options.
This is a minimally invasive surgery that is performed through a small incision in the rear limb.
The catheter is passed across the PDA from the femoral artery and a device (coil, plug, or occluder) is placed within the PDA.
This allows a blot clot to form that is eventually replaced with fibrous tissue, resulting in a permanent occlusion.