Role of Cardiac Computed Tomography Before Implant : Diagnosis of a Prominent Thebesian Valve as an Obstacle to Left Ventricular Lead Deployment in Cardiac Resynchronization Therapy

History

The patient had a medical history of hypertrophic cardiomyopathy with progression to the dilated phase of cardiomyopathy (New York Heart Association class III) and conduction abnormalities, including a prolonged QRS duration of 154 msec with right bundle branch block (RBBB) and left anterior fascicular block. Her family history was positive for hypertrophic cardiomyopathy in her father and one brother. Genetic testing revealed a mutation in the TNNI3 gene, resulting in replacement of the normal glutamic acid codon with a glutamine codon at position 124 in the troponin I gene. She had no history of hypertension, dyslipidemia, diabetes mellitus, or tobacco use. An echocardiogram demonstrated an ejection fraction of 20% to 25%. She underwent attempted cardiac resynchronization therapy defibrillator (CRT-D) implantation at a different institution, but the coronary sinus could not be cannulated. In addition, concern existed about possible coronary sinus dissection. Therefore a CRT-D device was implanted, with the left ventricular lead port capped. The patient was referred for evaluation for potential upgrade to a CRT-D via the implantation of the left ventricular lead. Cardiac computed tomography angiography (CCTA) was ordered for further evaluation of anatomic abnormalities impeding coronary venous lead placement.

Current Medications

The patient was taking carvedilol 6.25 mg in the morning and 12.5 mg at night, enalapril 7.5 mg daily, spironolactone 25 mg daily, furosemide 10 mg daily, and potassium chloride 10 mEq daily.

Physical Examination

• BP/HR: 90/56 mm Hg/60 bpm

• Height/weight: 165 cm/58 kg

• Neck veins: Jugular venous pressure 5 cm H ₂ O

• Lungs/chest: Lungs are clear to auscultation and percussion bilaterally; implantable cadioverter-defibrillator incision well healed

• Heart: Left ventricular impulse was laterally displaced; regular heart rate and rhythm; normal first heart sound (S ₁ ) and second heart sound (S ₂ ), without third heart sound (S ₃ ) or fourth heart sound (S ₄ ); 1/6 holosystolic murmur at the left lower sternal border radiating to the axilla

• Abdomen: Soft, nontender, nondistended; no evidence of hepatosplenomegaly, pulsatile abdominal masses, or abdominal bruits

• Extremities: Without clubbing, cyanosis, or edema

Laboratory Data

• Hemoglobin: 12.8 g/dL

• Hematocrit: 37.6%

• Mean corpuscular volume: 94 fL

• Platelet count: 119 cells/μL

• Sodium: 139 mmol/L

• Potassium: 3.9 mmol/L

• Creatinine: 0.9 mg/dL

• Blood urea nitrogen: 22 mg/dL

Electrocardiogram

Echocardiogram

A transthoracic echocardiogram showed mild left ventricular enlargement with wall thickness at the upper limits of normal and severe global hypokinesis with akinesis of the midinferior wall, inferior septum, and apex. The left ventricular ejection fraction was 22%, with a left ventricular end-diastolic dimension of 54 mm, a posterior wall thickness of 11 mm, and an interventricular septal thickness of 12 mm. Mildly decreased right ventricular systolic function was noted, as well as biatrial enlargement, with a left atrial volume index of 43 mL/m ² . The aortic valve was trileaflet, without aortic regurgitation or aortic stenosis. The mitral valve morphology was normal, with no evidence of mitral stenosis or regurgitation. No evidence of pulmonary regurgitation was seen. Trace tricuspid regurgitation was present, with an estimated right ventricular systolic pressure of 28 mm Hg. The right atrial pressure was estimated to be 5 mm Hg. The inferior vena cava size and respiratory variation were normal. No evidence of pericardial effusion was observed.

Cardiovascular Computed Tomographic Angiography