Further information: Normal and Abnormal Anatomy (see p205), Pathophysiology, Clinical Recognition, and Treatment of Congenital Heart Disease (see p233), Echocardiography in the Adult with Congenital Heart Disease (see p279), Congenital Heart Disease in the Adult: Interventional Therapy (see p311),  Surgical Treatment (see p341)   from Cardiovascular Medicine, 3rd Edn*

ESC Clinical Practice Guidelines for the Management of Grown-Up Congenital Heart Disease (2009) (ESC website accessed 08/27/10)   Full text

Further information: Congenital Heart Disease in the Adult: Interventional Therapy (see p311) from Cardiovascular Medicine, 3rd Edn*

One of the most controversial issues in cardiology in recent years has been to define the indications for closure of a patent foramen ovale (PFO). The newest indication for closure of the PFO has been to control migraine headaches. Not uncommon, PFOs have been found to occur in 10–25% of the population in the USA, and as much as 6% of the male population and 15–18% of the female population suffer from migraine headaches. Observational studies have suggested a pathophysiologic relationship in the prevalence of migraine headaches in patients who also have PFOs, and that closure of the PFO alleviated symptoms. In fact, the early studies came from a reported beneficial effect in the relief of migraine symptoms in patients who were undergoing closure for other indications.

The currently reported study [1] was the first large, prospective case-control study designed to test the association by using quantitative measures of migraine severity and core laboratory assessment of PFO with transthoracic echocardiography (TTE) and transcranial Doppler (TCD). Between August 2004 and December 2005, 360 subjects, 195 case subjects and 165 control subjects, were enrolled. Final matching yielded 144 subjects in each category for analysis. Odds ratios were calculated with conditional logistic regression in the matched cohort (n=288).

In the matched analysis, the prevalence of PFO was similar in case and control subjects (26.4% vs. 25.7%; odds ratio (OR) 1.04, 95% confidence interval (CI) 0.62–1.74, P=0.90). There was no difference in PFO prevalence in those with migraine with aura and those without (26.8% vs. 26.1%; OR 1.03, 95% CI 0.48–2.21, P=0.93). Therefore, no association between migraine headaches and the presence of PFO was found, and the investigators conclude that the focus should be on other mechanisms in the search to find the cause of migraine headaches.

In an editorial accompanying this article [2], the authors conclude that sufficient evidence does not exist for closure of a PFO for migraine to be considered standard medical practice and that further investigation into the mechanisms of migraine headaches is essential.

[1] Garg P, Servoss SJ, Wu JC, et al. Lack of association between migraine headache and patent foramen ovale. Circulation 2010;121:1406-12

[2] Gersony WM, Gersony DR. Migraine headache and the patent foramen ovale. Circulation 2010;121:1377-78

Patent Foramen Ovale and Cryptogenic Stroke in Older Patients

Further information: Congenital Heart Disease in the Adult: Interventional Therapy from Cardiovascular Medicine, 3rd Edn*

In 40% of patients who suffer a stroke, the cause is unidentified by routine diagnostic testing. However, one potential cause of embolic stroke is a patent foramen ovale (PFO) which allows right-to-left intracardiac shunting. Although the association between PFO and cryptogenic stroke has been studied in a population of younger patients (55 years of age or younger), there have been few studies and the association has remained unconfirmed in patients 55 years of age or older.

The present study [1] was conducted to determine if there were an association between the presence of PFO and cryptogenic stroke in patients 55 years of age or older and to compare the findings with those for younger patients. A total of 503 consecutive patients who had suffered a stroke were prospectively examined. The authors compared 227 patients with cryptogenic stroke and 276 control patients with stroke of known cause. There were 131 patients younger than 55 years old and 372 patients older than 55.

The authors found that the prevalence of PFO is significantly greater among patients with cryptogenic stroke than in patients with stroke of known cause for both younger patients (43.9% vs. 14.3%; odds ratio [OR], 4.70; 95% confidence interval [CI], 1.89–11.68; P<0.001) and older patients (28.3% vs. 11.9%; OR, 2.92; 95% CI, 1.70–5.01; P<0.001). A strong association was found between the presence of PFO with concomitant atrial septal aneurysm and cryptogenic stroke as compared with stroke of known origin, both in younger patients (13.4% vs. 2.0%; OR, 7.36; 95% CI, 1.01–326.60; P=0.049) and older patients (15.2% vs. 4.4%; OR, 3.88; 95% CI, 1.78–8.46; P<0.001). Multivariate analysis adjusted for age, plaque thickness, and the presence or absence of coronary artery disease and hypertension showed that the presence of PFO was independently associated with cryptogenic stroke in both the younger group (OR, 3.70; 95% CI, 1.42–9.65; P=0.008) and the older group (OR, 3.00; 95% CI, 1.73–5.23; P<0.001).

The authors concluded that there is an association between the presence of PFO and cryptogenic stroke in both older and younger patients. In evaluating the association between PFO and cryptogenic stroke in the older patient group, the authors noted that the probability of venous thromboembolism formation increases with increasing age and that a combination of the increased formation of thromboembloic material with hemodynamic changes that promote right-to-left shunting could contribute to increased paradoxical embolism in the older patient group.

[1] Handke M, Harloff A, Olschewski M, et al. Patent foramen ovale and cryptogenic stroke in older patients. N Engl J Med 2007;357:2262-68

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* To view the online text from the book, please navigate to SpringerLink or use the DVD to access electronic content. SpringerLink is a subscription service. For further information, click here.

Adolescent Overweight and Future Adult Coronary Heart Disease

Further information: Congenital Heart Disease in the Adult: Interventional Therapy from Cardiovascular Medicine, 3rd Edn*

Obesity has become a major health issue in the United States, and there are more that 9 million children and adolescents who are considered overweight. However, the effect of adolescent overweight on future adult coronary heart disease (CHD) is not understood.

The authors of this paper [1] used a computer-based system, the CHD Policy Model that is a computer simulation of CHD incidence, prevalence, mortality, and costs, used to estimate the potential impact of an increasingly overweight US adolescent population on future adult health. Data sources included the US census, the National Health and Nutrition Examination Surveys I, II, III, IV (NHANES), and the Copenhagen School Health Records Register (CSHR) to obtain data for the incidence of myocardial infarction (MI) and cardiac arrest.

Based on the prevalence of overweight adolescents in 2000, the researchers predicted that 30–37% of men and 34–44% of women will be obese by the year 2020 and that by 2035, the prevalence of CHD will increase by a range of 5–16% with more than 100,000 excess CHD cases attributable to this higher incidence of obesity. Researchers found that for boys, the elevated risk was significant at age 7 for both fatal events (adjusted hazard ratio [HR]: 1.10; 95% confidence interval [CI]: 1.06–1.15) and nonfatal events (adjusted HR: 1.05, 95%, CI: 1.03–1.08). Risk increased with age to HR of 1.24 and 1.17, respectively, at age 13. For girls, the elevated risk became significant at age 8 for fatal events (adjusted HR: 1.08, 95% CI: 1.01–1.17) and at age 10 for nonfatal events (adjusted HR: 1.06, 95% CI: 1.02–1.10). It also increased through age 13 to HR of 1.23 and 1.11, respectively.

On the basis of current known effects of obesity on cardiovascular risk factors, the projected effect of increased obesity on cardiovascular outcomes included: a) an excess total number of CHD events of 10% in 2020, rising to 14% in 2035 (absolute excess events 550 and 33,000, respectively; b) an excess CHD incidence of 15% by 2035 (40,000 events). However, the estimates would differ greatly if new treatments significantly changed obesity trends, prevention, or treatment of CHD, just as new treatments have significantly changed medicine. Such a reversal of the current trend would make the projections purely speculative.

[1] Bibbins-Domingo K, Coxson P, Pletcher MJ, et al. Adolescent overweight and future adult coronary heart disease. N Engl J Med 2007;357:2371-79

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* To view the online text from the book, please navigate to SpringerLink or use the DVD to access electronic content. SpringerLink is a subscription service. For further information, click here.

Corrections to figure legends:

Figure 9.22  This congenitally bifoliate aortic valve, photographed from above, shows the raphe on the aortic aspect of the conjoined leaflet.

Figure 9.23  This unicuspid and unicommissural valve, seen in an adult, has become calcified. It is the calcification of the leaflets, producing immobility that heralds the onset of symptoms.

Figure 9.24  This heart with hypertrophic cardiomyopathy has been sectioned to replicate the parasternal long axis echocardiographic section. Note the assymmetric septal hypertrophy and the ridge on the septal surface facing the aortic leaflet of the mitral valve.

Figure 9.28  The mural leaflet of this mitral valve lacks cordal support to the middle scallop which prolapses into the atrium.

Figure 9.43  In this heart, there is an aneurysm of the right coronary aortic sinus of Valsalva, which has been transilluminated from the aortic side, but is photographed from the right side. As can be seen, if the sinus ruptured, it would communicate with the right atrium.

ACC/AHA/ASE 2003 Guidelines for the Update for the Clinical Application of Echocardiography (Circulation. 2003;108:1146)   Summary article   Full text

ESC 2003 Management of grown up congenital heart disease (Eur Heart J 2003;24:1035-1084)   Full Text