Congenital Heart Diseases | Cardiology Clinical Questions | AccessCardiology

Does a patient with an atrial septal defect require closure?

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The decision to close an atrial septal defect (ASD) is based upon the size and degree of shunting.

HPI: May be asymptomatic. Dyspnea, exercise intolerance, palpitations.

PMH: Arrhythmias, pulmonary hypertension, congestive heart failure (CHF)

FH: Family History of congenital heart disease

May have a normal examination. Prominent right ventricular (RV) impulse, wide fixed splitting of S2, midsystolic pulmonary ejection murmur.

Prolonged PR interval.

Secundum ASD = Right axis deviation + right atrial enlargement + incomplete right bundle branch block (IRBBB).

Primum ASD = Left axis deviation + IRBBB.

Chest X-ray: RV and RA enlargement; prominent pulmonary artery; increased pulmonary vascularity.

Echocardiogram: Direct visualization of ASD or shunting (especially with agitated saline study), dilation of the right atrium/ventricle, elevated pulmonary pressure, Qp/Qs (pulmonary to systemic ratio) to quantitate shunt.

SYM = SYMptomatic ASD = Dyspnea on exertion, fatigue, palpitations, evidence of atrial arrhythmias.

ASYM = ASYMptomatic ASD

SIG-SHUNT = Significant left to right shunt (usually caught on echo), Qp:Qs > 1.5.

STR-CHANGE = Evidence of STRuctural CHANGEs in the heart such as elevated pulmonary pressure, right atrial or right ventricular enlargement or hypertrophy.

PxE = History of a paradoxical embolic event.

CLOSURE = CLOSURE of ASD. Can be performed percutaneously or surgically depending on size and location of ASD.

FOLLOW = Clinical follow up and echocardiogram every 2 years or sooner if symptoms develop.

END-STAGE = The clinical picture from an uncorrected significant ASD over time. May have severe irreversible pulmonary hypertension or Eisenmenger's physiology. Mortality is not improved with closure at this point. Prognosis is poor.

MED-TX = Medical management. There is no medicine to correct the anatomical defect. Can give medicines to alleviate right heart failure and pulmonary hypertension.

SYM + (NO END-STAGE) = CLOSURE

ASYM + SIG-SHUNT = CLOSURE

ASYM + STR-CHANGE = CLOSURE

ASYM + PxE = CLOSURE

ASYM + (NO SIG-SHUNT) + (NO STR-CHANGE) = FOLLOW

END-STAGE = MED-TX

Most patients with ASD are asymptomatic for decades and have a relatively normal physical exam making ASD the most common adult uncorrected congenital anomaly. The natural history for an ASD with a significant shunt is to develop pulmonary hypertension and right heart remodeling from pulmonary vascular overload. The mortality once severe pulmonary hypertension has developed is high. Closure of ASD has a very low incidence of morbidity and mortality from the procedure itself and can be done percutaneously or surgically. The goal is to close significant ASDs early before complications develop. Very small ASDs without significant shunting rarely become clinically significant.

– Closure is not recommended in patients with severe irreversible pulmonary artery hypertension.

– Most patients with ASD will be asymptomatic for decades.
– Mortality is increased with significant shunts due to pulmonary vascular overload, and can be improved with closure even when patients are older or asymptomatic.
– Once severe irreversible pulmonary hypertension has developed outcomes are not improved with closure.
– Small ASDs with trivial shunts usually are not clinically significant.

Warnes CA, Williams RG, Bashore TM, et. al. ACC/AHA 2008 Guidelines for Adults with CHD. J Am Coll Cardiol. 2008 Dec 2;52(23):e174–e176.
Brickner ME, et al. Congenital Heart Disease in Adults—First of Two Parts. N Engl J Med. 2000;342(4):256–263.
Du ZD, et al. Comparison Between Transcatheter and Surgical Closure of Secundum Atrial Septal Defect in Children and Adults: Results of a Multicenter Nonrandomized Trial. J Am Coll Cardiol. 2002;39(11): 1836–1844.

How do I manage my patient with a patent foramen ovale?

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The management of a patient with a patent foramen ovale (PFO) is based upon the risk of developing a cryptogenic stroke.

HPI: Syncope, paralysis, dyspnea, cyanosis, or migraine headache.

PMH: Thromboembolic event, cerebrovascular accident, hypercoagulable state (factor V Leiden, antithrombin deficiency, protein C and S deficiency), transient ischemic attack (TIA).

ECHO: Presence of right to left shunt across the interatrial septum with agitated saline contrast study.

PFO = Patient with documented Patent Foramen Ovale.

TIA = Patient with Transient Ischemic Attack.

CRST = Patient with prior CRyptogenic STroke (stroke occurring in the absence of an identified cardioembolic or large vessel source and with a distribution that is not consistent with small vessel disease).

HCS = HyperCoagulable State (factor V Leiden, antithrombin deficiency, protein C and S deficiency) or history of venous thromboembolism (deep venous thrombosis).

RCS = Patient with Recurrent Cryptogenic Stroke despite medical therapy.

ASP = ASPirin 325 mg/day.

AC = Oral AntiCoagulation with warfarin, target INR of 2–3.

CLOS = Refer patient for CLOSure of PFO.

PFO + TIA = ASA

PFO + CRST = ASA

PFO + HCS = AC

PFO + RCS = CLOS

Patients with a PFO are at an increased risk for the development of a cryptogenic stroke. Anticoagulation with warfarin is recommended in patients with a hypercoagulable state or history of venous thrombosis, as studies have shown the benefits outweigh the risks when compared to aspirin.

– PFO occurs in 25% of the general population.
– In patients <55 years with cryptogenic stroke, 46% were found to have a PFO.
– Patients with a larger size PFO have a higher recurrence rate of cryptogenic stroke.

Sacco RL, et al. Guidelines for Prevention of Stroke in Patients with Ischemic Stroke or Transient Ischemic Attack. Circulation. 2006;113:e409–e449.
Hidehiko H, et al. Patent Foramen Ovale: Current Pathology, Pathophysiology, and Clinical Status. J Am Coll Cardiol. 2005;46:1768–1776.

Should I refer my patient with an isolated ventricular septal defect for closure?

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The decision to refer a patient for closure of a ventricular septal defect (VSD) is based upon left ventricular function, degree of left to right shunting, pulmonary artery pressure, and presence of endocarditis.

HPI: Systolic murmur, dyspnea, orthopnea, or cyanosis.

PMH: Congestive heart failure, pulmonary artery hypertension.

Holosystolic murmur at left lower sternal border.

Biventricular hypertrophy or isolated right ventricular hypertrophy.

ECHO: Size and location of defect, number of defects, calculation of QP/QS, presence of left to right shunt, ventricular size and function.

X-ray: Left atrial and left ventricular enlargement, increased pulmonary vascular markings.

VSD = Patient with documented Ventricular Septal Defect.

CLOSURE = Refer patient for surgical CLOSURE of VSD.

QPQS = Pulmonary to systolic blood flow ratio (QP/QS) measured by echocardiogram or cardiac catheterization (normally in the absence of shunts, the flow through both pulmonary and system circulation should be the same so the QP/QS ratio should be 1.0).

LVOVD = Clinical evidence of Left Ventricular volume OVerloaD (usually noted as diastolic interventricular septal flattening resulting in a "D" shaped left ventricle on echocardiogram during diastolic relaxation).

IE = Patient with history of Infective Endocarditis.

L-R-S = Left to Right Shunting across VSD.

PAP = Pulmonary Artery Pressure less than two-thirds of systemic pressure.

PVR = Pulmonary Vascular Resistance less than two-thirds of systemic vascular resistance

LVF = Left Ventricular systolic or diastolic Failure.

VSD + QPQS >2.0 + LVOVD = CLOSURE

VSD + IE = CLOSURE

VSD + L-R-S + QPQS >1.5 + PAP + PVR = CLOSURE

VSD + L-R-S + QPQS >1.5 + PVR = CLOSURE

VSD + L-R-S + QPQS >1.5 + LVF = CLOSURE

Patients with VSD and elevated QP/QS, abnormal left ventricular function, or history of IE should be referred for surgical closure to prevent the development of pulmonary hypertension or Eisenmenger's syndrome.

– VSD closure is not recommended in patients with severe irreversible pulmonary artery hypertension.

– VSD is the most common congenital heart defect at birth.
– Seventy percent of VSDs are located in the membranous portion of the interventricular septum, with the majority of these closing spontaneously by the age of 12.

Warnes CA, et al. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease. J Am Coll Cardiol. 2008;52:e174–e176.
Brickner ME. Congenital Heart Disease in Adults. NEJM. 2000;342: 256–263.

Section VII: Congenital Heart Diseases

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Does a patient with an atrial septal defect require closure?

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