Heidi Connolly and Martha Grogan, MDs

Dr. Martha Grogan (left) presented on behalf of
Dr. Heidi Connolly (right) at ACC Lake Louise
due to last-minute circumstances.

Thanks very much to both of you this year!

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Drs. Grogan and Connolly are colleagues at Mayo Medical School in Rochester, Minnesota.

Martha Grogan is board-certified in internal medicine and cardiovascular diseases. She is a native of Cincinnati, Ohio, and received her medical degree from Northwestern University Medical School. Dr. Grogan has been on staff at Mayo Clinic since 1995 and is a consultant in the Division of Cardiovascular Diseases and is an assistant professor of medicine at Mayo Medical School.

Dr. Grogan is a noninvasive cardiologist specializing in heart failure, adult congenital heart disease and echocardiography. She has witnessed firsthand the importance of patient education in the treatment of diseases such as congestive heart failure and is excited about the tremendous educational opportunities now available through the Internet.

Heidi Connolly is a Professor of Medicine and a Consultant in Cardiovascular Diseases at Mayo Clinic.

She completed special training in Echocardiography and Adult Congenital Heart Disease and is Board Certified in both Internal Medicine and Cardiovascular Diseases.

Dr. Connolly is Director of the Congenital Heart Center and Co-Director of the Marfan and Thoracic Aortic Clinic at Mayo Clinic. She is an enthusiastic member of the Echocardiography Laboratory with special interests in congenital and intraoperative echo.

Additional clinical interests include valvular heart disease, carcinoid heart disease, and cardiac disorders in pregnancy.

Among other awards, Dr. Connolly has been recognized by the Mayo Cardiovascular Division Fellows for her teaching programs. She also received the United States Department of Health and Human Services FDA Commissioner’s Special Citation for her work on drug related valve disease.

PFO and Stroke: Guilt by Association

Tuesday, March 18, 2008
7:30 AM

Download Dr. Grogan’s conference slide set [19.0 MB PPT].
Download Dr. Connolly’s featured preconference slides [2.83 MB PDF].

The foramen ovale allows transfer of oxygenated placental blood to the fetal systemic circulation. This communication usually closes after birth. In 25-30% of the population, a potential pathway persists, and this is called a patent foramen ovale (PFO).

The association between PFO and stroke is controversial. Nearly one third of strokes are cryptogenic and PFO is commonly found in patients with cryptogenic stroke. Natural history studies suggest that PFO is not an independent predictor of cerebrovascular event after adjusting for age and comorbid conditions (1, 2). However, patients with both PFO and atrial septal aneurysm (ASA) who have had a stroke constitute a subgroup at substantial risk for recurrent stroke, and preventive strategies other than aspirin should be considered (3).

The outcome of a patient with PFO who has a cerebrovascular event and who does not receive treatment is unknown. The rationale for aspirin therapy comes from evidence that the small platelet/fibrin aggregates are the paradoxical particles associated with these events. The efficacy of aspirin therapy is suggested by the French PFO-ASA study, which found that among patients with a cryptogenic stroke who had a PFO alone, the incidence of a recurrent stroke on aspirin therapy was only 2.3% after four years, a value that was comparable to the 4.2% risk in patients with neither a PFO nor an ASA(3). WARSS demonstrated no significant benefit between warfarin and aspirin in the prevention of recurrent ischemic stroke or death or in the rate of major hemorrhage in patients with cryptogenic stroke (4). The PICSS study did not demonstrate a statistical difference between the effects of aspirin and warfarin on the risk of subsequent stroke or death among patients with cryptogenic stroke and PFO. However, this study was designed as a prognostic study and was underpowered to demonstrate a treatment effect (5).

Current data do not support routine PFO closure for primary prevention of stroke, cryptogenic stroke in a patient with PFO, asymptomatic large right-to-left shunt or recurrent migraine headaches. Clinical trials evaluating these relationships are underway.

Indications for PFO closure include embolic stroke or recurrent transient ischemic attack in a patient with a documented paradoxical embolus. PFO closure should also be considered for scuba divers with PFO, patients with cyanosis related to right-to-left shunt through a PFO due to tricuspid valve regurgitation, or platypnea orthodeoxia syndrome.

PFO closure can usually be safely performed by percutaneous intervention. Operative intervention may be preferable for a patient with multiple defects, hypercoagulable state, ASA with multiple fenestrations, or concomitant cardiac pathology.

References

1. Meissner, I, Khandheria, BK, Heit, JA, et al. Patent foramen ovale: innocent or guilty? Evidence from a prospective population-based study. J Am Coll Cardiol 2006; 47:440.
2. Petty, GW, Khandheria, BK, Meissner, I, et al. Population-based study of the relationship between patent foramen ovale and cerebrovascular ischemic events. Mayo Clin Proc 2006; 81:602.
3. Mas, JL, Arquizan, C, Lamy, C, et al. Recurrent cerebrovascular events associated with patent foramen ovale, atrial septal aneurysm, or both. N Engl J Med 2001; 345:1740.
4. Mohr JP, Thompson JLP, Lazar RM, et al. A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. N Engl J Med 2001; 345: 1444–1451
5. Homma S, Sacco RL, Di Tullio MR, et al. PFO in Cryptogenic Stroke Study (PICSS) Investigators. Effect of medical treatment in stroke patients with patent foramen ovale: patent foramen ovale in Cryptogenic Stroke Study. Circ 2002; 105: 2625-31.

Atrial & Ventricular Septal Defects: Identification & Management in the Adult

Tuesday, March 18, 2008
8:30 AM

Download Dr. Grogan’s conference slide set [13.0 MB PPT].
Download Dr. Connolly’s featured preconference slides [5.09 MB PDF].

There are four types of atrial septal defects (ASD). The most common is the secundum ASD (75%); this is usually an isolated congenital anomaly. Intervention is indicated when there is right-sided cardiac chamber enlargement and no pulmonary hypertension. Device closure should be considered in the absence of associated cardiac anomalies that require operative intervention. ASD closure is associated with an improvement in survival and symptoms; however the risk of atrial arrhythmias persists, the frequency is related to age at the time closure. The Holt Oram Syndrome and familial ASD associated atrioventricular conduction abnormalities are inherited forms of ASD.

Ostium primum ASDs (15% - 20%) are located in the lowest portion of the atrial septum. Part of the atrioventricular septal defect complex, these ASDs are usually associated with a cleft anterior mitral or tricuspid valve leaflet with associated valve regurgitation, a ventricular septal defect or aneurysm of the membranous ventricular septum, and left ventricular outflow tract obstruction. Operative intervention is the treatment of choice and should include closure of the ASD and cleft. These ASDs are common in Down syndrome.

Sinus venosus ASDs (5% - 10%) are located at the upper most portion of the atrial septum and are usually associated with one or more anomalous right-sided pulmonary veins. Transesophageal echocardiography is often required to confirm the diagnosis, and operative intervention is the treatment of choice. Inferior vena cava or unroofed coronary sinus ASDs are both very rare (< 1%). Anomalous pulmonary venous connection can cause right-sided volume overload without an ASD.

Ventricular septal defects (VSD) may be subdivided into 4 anatomical types according to their location on the ventricular septum. Muscular VSD’s can occur in any part of the ventricular septum and can be multiple. Spontaneous closure is common and although these defects account for up to 20% of VSDs in infants, the incidence is much lower in adults. Perimembranous VSDs are the most common accounting for ~80% of defects. They are located in the membranous portion of the ventricular septum adjacent to the septal leaflet of the tricuspid valve which can become adherent to the defect forming a pouch or “aneurysm” of the ventricular septum. This pouch will limit left-to-right shunting and can result in partial or complete closure of the VSD. The defect is also adjacent to the aortic valve. Inlet VSDs occur in the superior posterior portion of the ventricular septum, adjacent to the tricuspid valve. These defects are rare in adults, but do occur in patients with Down syndrome, and as part of the atrioventricular septal defect complex. Subpulmonary or outlet VSDs account for approximately 6% of defects in non-Asian populations, but up to 33% in Asian patients. Spontaneous closure of this type of VSD is uncommon and dilatation of the aortic sinus may cause aortic valve regurgitation.

VSD closure is recommended in adults with progressive aortic or tricuspid valve regurgitation, progressive left ventricular volume overload and occasionally for recurrent endocarditis. Device closure is possible in select VSDs.

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