Coronary reserve in volume-induced right ventricular hypertrophy from atrial septal defect

doi:10.1016/S0002-9149(84)80144-7

The American Journal of Cardiology

Volume 54, Issue 8, 1 November 1984, Pages 1059-1063

https://doi.org/10.1016/S0002-9149(84)80144-7 Get rights and content

To assess coronary reserve in patients with right ventricular (RV) hypertrophy secondary to volume overload, the quantitative characteristics of coronary reactive hyperemia were examined in 20 patients with a large atrial septal defect (ASD). The control group consisted of 13 patients who had undergone elective cardiac surgery for abnormalities that did not involve the right ventricle or its blood supply. Coronary blood flow velocity was measured in RV branches of the right coronary artery at cardiac surgery. Echocardiographic measurements of RV diameter in ASD and in control patients (2.3 ± 0.2 and 1.1 ± 0.2 cm, respectively, p <0.05) documented the presence of substantial RV enlargement in patients with ASD. In patients with ASD and in control subjects, a 20-second coronary occlusion produced maximal coronary dilation. After release of a 20 second coronary occlusion, the peak-to-resting velocity ratio in ASD and in control patients was 3.1 ± 0.2 and 5.5 ± 0.1, respectively (p <0.05). The 50% decrease in the ratio of peak-to-resting coronary blood flow velocity, a measure of relative coronary reserve, in patients with ASD suggests that coronary reserve is compromised in volume-induced RV hypertrophy. These studies support the concept that in humans, volume-induced RV hypertrophy substantially decreases coronary reserve.

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Cited by (28)

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Early electrical and geometric changes after percutaneous closure of large atrial septal defect
2004, American Journal of Cardiology
Citation Excerpt :
The “ideal” ASD treatment should aim at both eliminating the intracardiac shunt and at reverting the electrical and geometric changes caused by the cardiac overload. ASD surgery results in a significant improvement of symptoms,11,13 but often fails to completely revert the electrical and geometric cardiac abnormalities due to the long-standing volume overload. Despite significant changes in electrocardiographic signs of volume overload,14,15 most postsurgical patients continue to experience arrhythmias.16,17
Cardiac arrhythmias and right chamber enlargement are well known long-term sequelae of atrial septal defect (ASD). Surgical ASD closure relieves patient symptoms but often fails to revert cardiac volume overload findings. Transcatheter ASD closure might be an attractive alternative to surgery, also because of the possibility to study the amount and time-course of the electro-geometric modifications following shunt disappearance. Between March 2000 and December 2002, 24 patients (age 22.7 +16.8 years) underwent percutaneous closure of large ASD (stretched diameter >20 mm and/or QP/QS ratio >1.5:1). ASD closure was performed with the Amplatzer Septal Occluder device (mean 25 ± 7 mm), achieving a complete occlusion in all patients at 1 month. In 6 patients, right ventricular (RV) monophasic action potential was recorded during the procedure. All patients underwent standard 12-lead electrocardiography and transthoracic echocardiography before and at 24 hours and 1 month after ASD closure. After the procedure, monophasic action potential length increased from 359 ± 27 to 372 ± 27 ms (p <0.0001). At 1 month, QT dispersion decreased from 54 ± 25 to 41 ± 17 ms (p <0.05), RV diastolic diameter decreased from 42 ± 6 to 34 ± 5 mm (p <0.00001), and left ventricular (LV) diastolic diameter increased from 39 ± 5 to 44 ± 5 mm (p <0.0001), resulting in a decrease in the RV/LV ratio from 1.11 ± 0.22 to 0.79 ± 0.11 (−28.8%, p <0.00001). Electrocardiographic changes, as well as the amount and time-course of RV overload relief, did not significantly differ between pediatric (<16 years of age; n = 11) and adult patients (n = 13). In conclusion, regardless of age at procedure, percutaneous ASD closure results in early striking electrical and geometric cardiac changes that may be beneficial during long-term follow-up.
Myocardial flow reserve in patients with a systemic right ventricle after atrial switch repair
2001, Journal of the American College of Cardiology
Citation Excerpt :
These findings have been extended to the swine and to humans (26,27). In two additional human studies, which compared patients with pressure or volume-loaded RVs to control subjects with normal RVs, myocardial flow reserve values in control RVs were similar to the known values of LV myocardial flow reserve in the normal young population (21,28). Therefore, we believe that the LV MBF in healthy subjects is acceptable for comparison with MBFs and flow reserve in this study population.
OBJECTIVES
The purpose of this study was to assess myocardial blood flow (MBF) and flow reserve in systemic right ventricles (RV) in long-term survivors of the Mustard operation.
BACKGROUND
There is a high prevalence of systemic RV dysfunction and impaired exercise performance in long-term survivors of the Mustard operation. A mismatch between myocardial blood supply and systemic ventricular work demand has been proposed as a potential mechanism.
METHODS
We assessed MBF at rest and during intravenous adenosine hyperemia in 11 long-term survivors of a Mustard repair (age 18 ± 5 years, median age at repair 0.7 years, follow-up after repair 17 ± 5 years) and 13 healthy control subjects (age 23 ± 7 years), using N-13 ammonia and positron emission tomography imaging.
RESULTS
There was no difference in basal MBF between the systemic RV of survivors of the Mustard operation and the systemic left ventricle (LV) of healthy control subjects (0.80 ± 0.19 vs. 0.74 ± 0.15 ml/g/min, respectively, p = NS). However, the hyperemic flows were significantly lower in systemic RVs than they were in systemic LVs (2.34 ± 0.0.69 vs. 3.44 ± 0.62 ml/g/min respectively, p < 0.01). As a result, myocardial flow reserve was lower in systemic RVs than it was in systemic LVs (2.93 ± 0.63 vs. 4.74 ± 1.09, respectively, p < 0.01).
CONCLUSIONS
Myocardial flow reserve is impaired in systemic RVs in survivors of the Mustard operation. This may contribute to systemic ventricular dysfunction in these patients.

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^*: These studies were supported by Grant HL 20827 and Program Project Grant HL 14388 from the National Heart, Lung and Blood Institute, Bethesda, Maryland, and research funds from the Veterans Administration.

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Coronary reserve in volume-induced right ventricular hypertrophy from atrial septal defect*

Coronary artery luminal diameters in normal and hypertrophied canine ventricles (abstr)

Circulation

Interarterial coronary anastomoses in the human heart, with particular reference to anemia and relative cardiac anoxia

Circulation

Coronary circulation in the normal and the pathologic heart

Quantitative morphology of capillaries of the heart. Number of capillaries in animal and human hearts under normal and pathological conditions

Arch Exp Pathol

The extent of the capillary bed of the heart

J Exp Med

Left ventricular vascularity in the hypertrophied heart (abstr)

Physiol

Coronary blood flow in experimental canine left ventricular hypertrophy

Circ Res

Effect of renal hypertension and left ventricular hypertrophy on the coronary circulation in dogs

Circ Res

Reduction of maximal coronary vasodilator capacity in conscious dogs with severe right ventricular hypertrophy

Circ Res

Transmural distribution of myocardial blood flow and of coronary reserve in canine left ventricular hypertrophy

Basic Res Cardiol

Regional myocardial blood flow in developing cardiac hypertrophy (abstr)

Circulation

Myocardial blood flow distribution in concentric left ventricular hypertrophy

J Clin Invest

Regional myocardial blood flow during exercise in dogs with chronic left ventricular hypertrophy

Circ Res

Measurements of coronary velocity and reactive hyperemia in the coronary circulation of man

Circ Res