CLINICAL STUDY: CARDIOMYOPATHY
Isolated ventricular noncompaction is associated with coronary microcirculatory dysfunction
Rolf Jenni, MD, MSEE*,
Christophe A. Wyss, MD ,
Erwin N. Oechslin, MD* and
Philipp A. Kaufmann, MD,*
* Department of Echocardiography, Cardiovascular Center, University Hospital, Zurich, Switzerland
Department of Nuclear Cardiology, Cardiovascular Center, University Hospital, Zurich, Switzerland
Manuscript received July 18, 2001;
revised manuscript received October 15, 2001,
accepted November 1, 2001.
* Reprint requests and correspondence: Dr. Philipp Kaufmann, Head of Nuclear Cardiology, Cardiovascular Center C NUK 32, University Hospital, Ramistr. 100, CH-8091 Zurich, Switzerland.
Philipp.Kaufmann{at}dmr.usz.ch
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Abstract
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OBJECTIVES: We sought to analyze whether a microcirculatory dysfunction might be associated with isolated ventricular noncompaction (IVNC).
BACKGROUND: In IVNC, which is a cardiomyopathy thus far "unclassified" by the World Health Organization, heart failure and sudden cardiac death are common findings, but the pathophysiologic mechanisms are unknown.
METHODS: In 12 patients with IVNC and 14 control subjects, quantitative evaluation of regional myocardial perfusion (myocardial blood flow [MBF]) and coronary flow reserve (CFR, hyperemic/baseline MBF) was performed using positron emission tomography and 13N-ammonia. The left ventricular myocardium was divided into nine segments, and the two-dimensional echocardiogram in each patient with IVNC was compared with CFR in each segment. Noncompaction was defined as a two-layered structure with excessive trabeculation.
RESULTS: The CFR in control subjects averaged 4.2 ± 0.9, providing a cut-off value  2.5, but it was 2.1 ± 0.8 in patients with IVNC. A perfusion scan defect was found in 14 of 24 segments with noncompaction, although no defect was found in 76 of 84 normal segments (overall agreement 83%, p < 0.0001 by the chi-square test). In 16 of 21 segments with noncompaction, a decreased CFR was found; but a decreased CFR was also found in 36 of 60 segments without noncompaction (p = NS). In 45 of the 57 segments with wall motion abnormalities, CFR was decreased, but it was preserved in 17 of the 24 segments with normal wall motion (agreement 77%, p < 0.0001).
CONCLUSIONS: In patients with IVNC, a decreased CFR is not confined to noncompacted segments, but extends to most segments with wall motion abnormalities. Thus, coronary microcirculatory dysfunction is associated with IVNC.
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Abbreviations and Acronyms
| | NYHA | | CFR | | coronary flow reserve | | IVNC | | isolated ventricular noncompaction | | LV | | left ventricular or ventricle | | MBF | | myocardial blood flow | | PET | | positron emission tomography | | ROI | | region of interest | | WHO | | World Health Organization |
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According to the present World Health Organization (WHO) definition, cardiomyopathies are now classified by the dominant pathophysiology or, if possible, by etiologic/pathogenetic factors (1). As the etiology of isolated ventricular noncompaction (IVNC) is not fully elucidated, IVNC has been unspecifically assigned to a heterogeneous group of "unclassified cardiomyopathies." The disease is thought to be a morphogenetic abnormality involving an arrest of compaction of the loose myocardial meshwork during fetal ontogenesis (2,3), thus, present at birth in all patients (4,5).
Heart failure, arrhythmia, embolism and sudden cardiac death are common clinical manifestations of IVNC (6,7). Chest pain was found in 26% of patients with IVNC (7). Echocardiographic characteristics of IVNC have been validated at autopsy and include, in the absence of any coexisting lesion, segmental thickening of the left ventricular (LV) myocardial wall consisting of two layers (Fig. 1, left): a thin, compacted epicardial layer and an extremely thick endocardial layer with prominent trabeculations and deep recesses (8). The pathophysiology of myocardial perfusion may play a crucial role in IVNC, with ischemia possibly resulting from underlying abnormalities of the coronary microcirculation, as suggested by postmortem analyses of IVNC hearts with ischemic subendocardial lesions (7,8).
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Figure 1 Mid-ventricular short-axis view of an echocardiographic recording (left) showing septal, inferior and lateral hypertrabeculation and a two-layered structure of the left ventricular myocardium, indicative of noncompaction. The corresponding nongated 13N-ammonia scan (right) shows lateral and inferior irregularities. PET = positron emission tomography.
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We hypothesized that these findings may originate in, or at least be partly due to, a functional impairment of the coronary microcirculation. The purpose of the present report was to study whether IVNC is associated with a microcirculatory dysfunction.
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Methods
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Study group.
A total of 12 patients, derived from a previously reported series of 34 patients with IVNC (7), was studied (mean age 49 ± 18 years). The diagnostic criteria for IVNC have been validated at autopsy (8). Briefly, IVNC is characterized by a two-layer structure with a compacted, thin epicardial band and a much thicker, noncompacted endocardial layer of trabecular meshwork with deep endomyocardial spaces and color Doppler evidence of deep perfused intertrabecular recesses. A maximal end-systolic ratio of noncompacted to compacted layers of >2 is diagnostic. The patients were chosen consecutively on their scheduled routine visit to the outpatient clinic. Seven of the reported patients had shortness of breath (4 patients in New York Heart Association functional class II and 3 patients in class III) and two had chest pain. Left bundle branch block was present in three patients and repolarization abnormalities in four patients. Cardiovascular risk factors were present in three patients. Four patients, including the two with chest pain, had undergone coronary angiography, which revealed normal coronary arteries.
Fourteen volunteers without cardiovascular disease served as control subjects (mean age 34 ± 15 years; p < 0.01 vs. patients with IVNC). None of the control subjects had a history of cardiovascular disease or risk factors. Entrance criteria included a normal heart rate, normal blood pressure, a normal rest electrocardiogram and a low clinical probability of coronary artery disease (9).
Positron emission tomography.
Positron emission tomographic (PET) studies were performed with a GE Advance PET scanner (GE Medical Systems, Milwaukee, Wisconsin; axial field of view 35 x 4.25 mm). All volunteers were injected with 700 to 900 MBq of 13N-ammonia into a peripheral vein by the bolus technique, while acquisition of the serial transaxial tomographic images of the heart was started (12 x 10-s, 4 x 30-s, 1 x 60-s and 2 x 300-s frames). After 20-min acquisition, a 20-min transmission scan for photon attenuation correction was performed using external 68Ge sources. Myocardial blood flow (MBF) was assessed at rest and during standard pharmacologic stress (i.e., dipyridamole in control subjects and adenosine in patients with IVNC). Both dipyridamole and adenosine have been shown to induce equivalent hyperemia at the applied intravenous dose and rate (10).
Data analysis.
The heart was divided into nine segments: the whole apex was one segment (apical segment), and at the base and mid-ventricular levels, the LV was divided into four segments each—septal, anterior, lateral and inferior. A region of interest (ROI) was placed in each segment, as well as into the LV blood pool.
Myocardial blood flow was estimated by model fitting of the blood pool and myocardial time–activity curves (11). Correction for partial volume and spillover (both accounting for the resolution distortion) was performed using the method developed (12) and validated by Hutchins et al. (13). Briefly, the ROI was chosen to contain only myocardial tissue and blood; thus, the relationship between the measured PET counts in a region (CPET) and the true counts in myocardium (Cm) and arterial blood (Ca) was modeled as follows: CPET(t) = FaCa(t) + (1 – Fa)Cm(t), where Fa is the fractional contribution of the blood pool to measured PET counts in a region and is dependent on the placement of the region, the resolution of the camera and the movement of the myocardium. Because the contribution of the myocardium to total regional counts decreases with an increasing blood pool fraction, Cm is multiplied by (1 – Fa). Fa was estimated, together with the other kinetic tissue variables, by using least-squares fitting. Determination of the fraction of the ROI volume occupied by blood (Fa) by either measurement or variable estimation procedures eliminates the resolution distortion in the kinetic data. This strategy of spillover correction seems to be the most appropriate in light of the depth of the sinusoids in IVNC. Coronary flow reserve (CFR) was calculated as the ratio of hyperemic to rest MBF values. The images of the last 300-s frame were used to grade each segment as a normal perfusion scan or a defect for rest and stress.
Echocardiography.
Two-dimensional and Doppler echocardiographic studies were performed in patients with IVNC, according to the recommendations of the American Society of Echocardiography (14–16). The LV ejection fraction was calculated using the biplane area–length method (17). The LV wall was divided into nine segments to describe the location of the noncompacted segments: the whole apex was one segment (apical segment) and at the base and mid-ventricular levels, the LV was divided into four segments each—septal, anterior, lateral and inferior. Systolic function was graded as normal or abnormal (i.e., hypokinetic, akinetic or dyskinetic segment). The echocardiographic data were scored by an operator who had no knowledge of the PET data and reported in Table 1. The study protocol was approved by the institutional Research Ethics Committee.
Statistical analysis.
Statistical comparisons of hemodynamic data, MBF and CFR were carried out by one-way analysis of variance for repeated measures. When the analysis was significant, the Sheffé F test was applied. Data are reported as the mean value ± SD. The chi-square test was used for categorical analysis of nominal data.
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Results
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All procedures were well tolerated, except in one IVNC patient in whom adenosine stress testing had to be discontinued because of common side effects, such as dyspnea and chest pain.
Hemodynamic data.
Heart rate, systolic and diastolic blood pressure and the rate–pressure product were comparable in both groups. Using dipyridamole and adenosine stress, the heart rate increased significantly in both groups, except in one patient with IVNC (nonresponder, as described in the following text).
Myocardial blood flow and CFR.
Hyperemic MBF could not be analyzed in three patients with IVNC (one nonresponder to adenosine, one who had a technical problem and one in whom adenosine was discontinued due to side effects); the remaining nine patients with IVNC (mean age 45 ± 17) underwent quantitative analysis. Global MBF at baseline was similar between control subjects (0.78 ± 0.25 ml/g per min) and patients with IVNC (0.86 ± 0.30 ml/g per min; p = NS). Dipyridamole induced a significant increase in MBF in control subjects (3.18 ± 1.23 ml/g per min; p < 0.0001 vs. baseline), whereas the hyperemic response was significantly reduced in patients with IVNC (1.72 ± 0.75 ml/g per min, p < 0.0005 vs. patients with IVNC). Global CFR was 4.21 ± 0.86 for control subjects, resulting in a cutoff value (mean –2 SD) of <2.49 for reduced CFR. In patients with IVNC, CFR was significantly reduced, as compared with that in control subjects (2.13 ± 0.83; p < 0.001 vs. control subjects). In patients with IVNC, all segments were categorized as having a normal (2.5) or decreased (<2.5) CFR.
Echocardiography and PET.
Trabeculation was most commonly found in the apical and mid-ventricular lateral wall, followed by the mid-ventricular inferior wall, as previously reported (7,8). All noncompacted segments, but also 35 of 60 normally compacted segments, were hypokinetic. In patients with IVNC, a fixed perfusion scan defect was found in 14 of 24 segments with noncompaction, whereas normal perfusion was found in 76 of 84 segments without trabeculation (overall agreement 83%, p < 0.0001 by the chi-square test). In 16 of 21 segments with noncompaction, a decreased CFR was found, but a decreased CFR was also found in 36 of 60 segments without trabeculation (p = NS).
In 45 of the 57 segments with wall motion abnormalities, CFR was decreased, whereas CFR was normal in 17 of the 24 segments with normal wall motion (agreement 77%, p < 0.0001) (Fig. 2). For the echocardiographic findings in patients with IVNC, see Table 1.
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Figure 2 Comparison between echocardiography and positron emission tomography in patients with isolated ventricular noncompaction. The microcirculatory dysfunction is not confined to noncompacted segments (right and middle), but extends to most myocardial segments with wall motion abnormalities (left). Perfusion defects were assessed in 12 patients (108 segments); quantification was successful in only nine patients (81 segments). CFR = coronary flow reserve.
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Discussion
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Assessment of microcirculatory dysfunction in patients with IVNC.
Isolated ventricular noncompaction is a rare and unique congenital disorder categorized as an unclassified cardiomyopathy by WHO in 1995. Despite an increasing interest in this congenital anomaly in the past decade, as reflected by several recent reports (4–7,18–21), following the initial publications (2,3), the pathophysiologic mechanisms of LV dysfunction in patients with IVNC remains unclear. To the best of our knowledge, this is the first systematic report to provide evidence for an underlying microcirculatory dysfunction in IVNC. A decreased rest and hyperemic MBF has previously been found in a case report of five children with IVNC, but without statistical analysis, as MBF was only successfully quantified using PET in three patients (22). Our results in adults with IVNC demonstrate a preservation of MBF at rest, but a significantly impaired increase in MBF during maximal hyperemia with adenosine, resulting in a decreased CFR. We have used a strategy for placement of the myocardial ROI in the PET scan, which proposes the inclusion of myocardial tissue as well as the LV blood pool (12,13). This seems appropriate for analyzing patients with IVNC with deep recesses, because any such model needs to correct for an admixture of perfused muscle with vasodilation and blood in the recesses without vasodilation. Thus, the observed lack of a flow increase in IVNC is unlikely to simply reflect a partial volume effect.
Relationship between microcirculatory dysfunction and wall motion abnormalities.
Coronary flow reserve, defined as the ratio of near maximal to basal myocardial flow, has been proposed as an indirect variable to evaluate the function of the coronary circulation (23). It is an integrated measure of coronary flow through both the large epicardial coronary arteries and the microcirculation. A decrease in CFR can be due to narrowing of epicardial coronary arteries (24), which is, however, unlikely in our group of patients with IVNC, as previously documented (3,6,7), or to a microvascular dysfunction (25). A similar microcirculatory dysfunction has been reported in other cardiomyopathies. In hypertrophic obstructive cardiomyopathy, an impaired coronary vasodilator reserve, as assessed with PET, has been found in both hypertrophied and nonhypertrophied regions of the LV, suggesting that ischemia may result from abnormalities of the coronary microcirculation (26). Similarly, in IVNC, the microcirculatory dysfunction was not confined to the trabeculated segments, but was found to extend to many nontrabeculated segments. This indicates that the hypertrophy, per se, is unlikely to account for the decreased CFR, as the latter was also found in nonhypertrophied segments. In most of these segments, a wall motion abnormality was found. In contrast, however, in most of the segments without a wall motion abnormality, a normal CFR was preserved. This provides evidence that the microcirculatory dysfunction may be associated with wall motion abnormalities and, thus, with heart failure in patients with IVNC. The causal relationship between microcirculatory and contractility dysfunction in IVNC cannot be identified with certainty by our observational study. However, it appears reasonable to assume that the microvascular dysfunction might be responsible for the contractile impairment, particularly during high-demand situations, explaining the subendocardial scar, as found in histologic preparations of patients with IVNC (8), and reflected by fixed ammonia defects in our study, despite no evidence of a previous myocardial infarction. Recently, impaired aerobic fatty acid metabolism has been found in noncompacted segments, supporting the hypothesis that myocardial failure in IVNC may be a result of ischemia (27).
Study limitations.
Patients with IVNC were slightly older than control subjects. This difference may potentially hamper the comparability of the two groups’ flow reserve, as the maximal hyperemic response decreases significantly after the age of 70 years, and the flow reserve has been shown to decrease after the age of 60 years (28), mainly due to an increase in basal flow (29). However, only two of our patients were >60 years, and the baseline flow was not increased in patients with IVNC as compared with control subjects. Thus, the significant decrease in CFR in patients with IVNC cannot be explained by the slight age difference.
Although equipotent doses of the two stressors, adenosine and dipyridamole (10), have been used, resulting in the same hyperemic MBF values on PET (30), a slightly stronger hyperemic effect of adenosine over dipyridamole has recently been reported (31). Therefore, adenosine would overestimate CFR. As this was used in patients with IVNC who had decreased CFR values, this would even strengthen our results.
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Footnotes
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Dr. Kaufmann was funded by a grant from the Swiss National Science Foundation (SCORE B grant no. 32-55002.98). This work was supported by the EMDO Stiftung Zurich and the Radiumfonds für Krebsforschung, Switzerland.
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R. H. Pignatelli, C. J. McMahon, W. J. Dreyer, S. W. Denfield, J. Price, J. W. Belmont, W. J. Craigen, J. Wu, H. El Said, L. I. Bezold, et al.
Clinical Characterization of Left Ventricular Noncompaction in Children: A Relatively Common Form of Cardiomyopathy
Circulation,
November 25, 2003;
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[Abstract]
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C. A. Wyss, P. Koepfli, K. Mikolajczyk, C. Burger, G. K. von Schulthess, and P. A. Kaufmann
Bicycle Exercise Stress in PET for Assessment of Coronary Flow Reserve: Repeatability and Comparison with Adenosine Stress
J. Nucl. Med.,
February 1, 2003;
44(2):
146 - 154.
[Abstract]
[Full Text]
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Abstract
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