ABSTRACT
Background
A detailed evaluation of hemodynamics, supportive morphology, and deformation may help uncover the pathophysiology of hypertrophic obstructive cardiomyopathy (HOCM) and the changes wrought by alcohol septal ablation (ASA).
Purpose
To investigate the global cardiac volume, myocardial deformation, and hemodynamic characteristics before and during long‐term follow‐up after ASA in patients with HOCM.
Study Type
Retrospective.
Subjects
Twenty‐three patients (68.1 ± 8.6 years, 21.7% male) with HOCM who underwent MRI before and after ASA.
Field Strength/Sequence
A 3T, Two‐dimensional fast imaging employing steady‐state acquisition, inversion recovery‐prepared fast gradient echo sequences, and cine and time‐resolved three‐dimensional cine phase‐contrast (4D flow) MRI.
Assessment
Global left ventricular (LV) volume by cine, peak strain, and strain rate by myocardial feature‐tracking MRI, and hemodynamic characteristics by 4D flow MRI.
Statistical Tests
Paired t‐test and Wilcoxon signed–rank test compared normally and nonnormally distributed data, respectively. Chi‐squared or Fisher's exact tests were used to compare categorical data, as appropriate. Pearson's or Spearman's correlation coefficient evaluated the correlations. Statistical significance was set at q ≤ 0.10 or p < 0.05.
Results
In LV long‐axis images, the global radial strain increased significantly (16.6% ± 5.8% vs. 20.1% ± 6.8%), whereas the global longitudinal strain decreased significantly after ASA (−10.5% ± 3.2% vs. −12.1% ± 3.5%). The diastolic LV anterior vortex area increased significantly after ASA (2256.1 [703.6, 4038.4] vs. 3826.1 [1914.3, 4820.1] mm2). Multiplication of the LV end‐diastolic volume index, global circumferential strain, and diastolic radial peak strain rate in LV long‐axis images revealed a significant correlation with the diastolic LV anterior vortex area (Rs = 0.43).
Data Conclusions
Feature‐tracking and 4D flow MRI revealed improved systolic and diastolic LV function during long‐term follow‐up after ASA. The diastolic LV vortex was associated with the combined parameters of LV volume and deformation. Comprehensive cardiac MRI may help understand the beneficial effects of ASA.
Evidence Level
3.
Technical Efficacy
Stage 5.
Keywords: alcohol septal ablation, four‐dimensional flow magnetic resonance imaging, hypertrophic obstructive cardiomyopathy, strain, strain rate
Plain Language Summary
We studied patients with hypertrophic obstructive cardiomyopathy (HOCM), a heart disease that thickens the heart muscle and blocks blood flow. A treatment called alcohol septal ablation (ASA) can relieve this blockage, but its long‐term effects on heart function are not fully understood. Using advanced MRI techniques, we examined heart shape, pumping ability, and blood flow before and several years after ASA in 23 patients. We found that heart muscle motion and blood flow patterns improved after treatment, helping the heart pump and fill more efficiently. These findings show that MRI can reveal how ASA benefits patients over time.
1. Introduction
Hypertrophic obstructive cardiomyopathy (HOCM) is a common phenotype of hypertrophic cardiomyopathy [1] that may lead to heart failure or syncope, resulting in a poor prognosis [2]. HOCM is morphologically characterized by basal septal hypertrophy, elongated mitral valve (MV) leaflets, abnormal sub‐MV apparatus, and associated systolic anterior motion (SAM), resulting in left ventricular (LV) outflow tract (LVOT) obstruction [1, 3]. Alcohol septal ablation (ASA), a catheter‐based septal reduction therapy for drug‐refractory HOCM, can alleviate heart failure symptoms and improve prognosis [4, 5, 6]. Without directly impacting the MV, ASA can reduce SAM. Elucidating the mechanisms of SAM development in HOCM and its control by ASA is thus important. A detailed evaluation of hemodynamics, supportive morphology, and deformation may help uncover the pathophysiology of HOCM and the changes wrought by ASA, which may further improve patient management.
Time‐resolved three‐dimensional cine phase‐contrast (4D flow) MRI can be used to visualize and quantify three‐dimensional blood flow in vivo [7, 8]. Studies on patients with HOCM have investigated the ascending aorta (AAO) flow pattern [9], turbulent kinetic energy [10], and energy loss [11]; however, the intra‐LV flow pattern has rarely been investigated [12]. Although a previous study evaluated intra‐LV hemodynamics 1 week after ASA [13], the long‐term stabilized hemodynamics after ASA have not been investigated. Recently, myocardial feature tracking (FT) using conventional cine images has enabled deformation analysis, providing more precise distinctions in local myocardial motion through strain‐related parameters [14]. Consequently, the predictive values of cardiac MRI‐derived strain‐related parameters for patients with hypertrophic cardiomyopathy have been reported [15, 16, 17, 18]. However, the effects of deformation on hemodynamic parameters remain unclear.
Conventional imaging and hemodynamic assessment cannot fully capture the complex interplay between abnormal myocardial deformation and disturbed intraventricular flow in HOCM. ASA may improve symptoms not only by reducing the LVOT gradient but also by modifying intra‐LV flow dynamics and myocardial mechanics. 4D flow MRI can visualize and quantify this altered hemodynamics, while FT enables sensitive detection of subtle regional dysfunction. Therefore, a combined evaluation of deformation and 4D flow may provide unique insights into the mechanisms of symptom relief after ASA and offer novel markers for risk stratification in this population.
This study aimed to investigate the changes in global cardiac function by cine MRI, deformation by FT MRI, and hemodynamics by 4D flow MRI before and during long‐term follow‐up after ASA, and the correlations among cardiac volume, deformation, and hemodynamics in patients with HOCM.
2. Materials and Methods
2.1. Study Design
This study was conducted in accordance with the Declaration of Helsinki and was approved by the institutional review board. All patients provided written informed consent.
The patient selection process for this single‐center, retrospective observational study is summarized in Figure 1. Patients with HOCM who underwent ASA between February 2018 and September 2023 and had both baseline and follow‐up cardiac MRI data were included in the study. Patients were excluded if they had cardiac implantable electronic devices, renal dysfunction, or were diagnosed with HOCM only after cardiac MRI and therefore did not undergo 4D flow MRI. Baseline characteristics, including demographic data, heart failure symptoms according to the New York Heart Association functional classification, medical history, medications, laboratory results, and echocardiographic findings, were collected at diagnosis. Characteristics of the ASA procedure were also assessed.
FIGURE 1.
Flowchart of patient enrolment. 4D, four‐dimensional; ASA, alcohol septal ablation; CIED, cardiac implanted electric device; HOCM, hypertrophic obstructive cardiomyopathy; MRI, magnetic resonance imaging.
2.2. MRI
MRI was performed using a 3T scanner (Discovery MR750 or MR750w; GE Healthcare, Waukesha, WI, USA) for all patients before and after ASA, with a maximum gradient strength of 50 mT/m (MR750) or 44 mT/m (MR750w) and a maximum slew rate of 200 mT/m/ms (both MR750 and MR750w). A commercially available 32‐channel phased‐array body coil for MR750 or the geometry embedding method phased‐array coil for MR750w was applied. Two‐dimensional (2D) fast imaging employing steady‐state acquisition (FIESTA) based on a steady‐state free precession sequence for cine images was performed on short‐axis (SAX) and 2‐chamber, 3‐chamber, and 4‐chamber long‐axis (LAX) orientations with a slice thickness and gap of 10 mm and 0 mm, respectively. Inversion recovery‐prepared fast gradient echo sequences for late gadolinium enhancement (LGE) images were acquired in SAX, 2‐chamber LAX, and 4‐chamber LAX orientations with a slice thickness and gap of 10 mm and 0 mm, respectively. A bolus of 0.1 mmol/kg gadobutrol (Gadovist, Bayer AG, Berlin, Germany) was injected using a power injector (Sonic Shot GX, Nemoto Kyorindo Co., Tokyo, Japan).
2.3. 4D Flow MRI Acquisition and Postprocessing
Retrospective electrocardiogram (ECG)‐gated 4D flow MRI data were acquired via a respiratory navigator with full volumetric coverage of the whole heart and AAO. The imaging parameters for the 4D flow MRI were as follows: repetition time (TR): 4.7 ms, echo time (TE): 2.4 ms, flip angle (FA): 15°, number of excitations (NEX): 4, field of view (FOV): 32–36 cm, matrix: 224 × 224, thickness: 2 mm, partitions: 60, phases during one cardiac cycle: 20, velocity sensitivity (VENC): 550 cm/s, and receiver bandwidth (RBW): 62.5 kHz. Velocity sensitivity (VENC) was set at 550 cm/s not to miss the accelerated blood flow associated with outflow tract obstruction. The data were reconstructed by autocalibrating reconstruction for Cartesian sampling with a reduction factor of two on a personal computer (Intel Xeon E3‐1270 [3.4 GHz/Quad‐core] DDr3, 16 GB ECC, Linux). For geometric information of 4D flow MRI data, multiphase contrast‐enhanced 3D fast spoiled gradient recalled acquisition in the steady state (FSPGR) MR angiography (MRA) was performed. The imaging parameters for the coronal MRA were as follows: TR: 3.2 ms, TE: 1 ms, FA: 12°, NEX: 1, FOV: 32–36 cm, size of the reconstructed matrix with the aid of zero‐fill interpolation: 512, RBW: 83.3 kHz, and imaging time: 33 s for the four phases.
2.4. Cardiac Volume, Strain, and LGE
Conventional cardiac volume indexed by body surface area, function, and strain in the left ventricle (LV), right ventricle (RV), and left atrium (LA) were analyzed with 2D FIESTA images by K.S. (14 years of MRI experience) using cvi42 (Circle Cardiovascular Imaging Inc., Calgary, Canada). The LV end‐diastolic volume index, LV end‐systolic volume index, LV stroke volume index, LV cardiac index, LV ejection fraction, LV mass index, RV end‐diastolic volume index, RV end‐systolic volume index, RV stroke volume index, RV cardiac index, and RV ejection fraction were quantified via SAX 2D FIESTA images. The minimum LA volume index, maximum LA volume index, and LA empty fraction were quantified using 2‐chamber and 4‐chamber LAX 2D FIESTA images. The amount of LGE was quantified as the LGE mass and %LGE, a fraction of the LGE mass to the LV mass, with a threshold of > 5 standard deviations of remote myocardium according to SAX images. The strain and peak strain rate (SR) were assessed using the FT technique. For the LV and RV, 2D global radial strain (2D‐GRS) and 2D global circumferential strain (2D‐GCS) were evaluated using SAX images, and 2D‐GRS and 2D global longitudinal strain (2D‐GLS) were assessed in LAX images. Local peak strain in the American Heart Association 16‐segment model was measured for the LV. The average LAX strain and average LAX difference were quantified for LA. The 2D radial and circumferential peak SRs in the SAX images and radial and longitudinal peak SRs in the LAX images were measured for systole and diastole.
2.5. Hemodynamic Assessment Using 4D Flow MRI
The 3D segmentation of the heart and vessel structures and visualization and quantification of hemodynamic measurements for 4D flow MRI were performed using Flova (R'‐Tech, Hamamatsu, Japan) software. For the segmentation of the volume of interest, we used anatomical structures in diastole as a static reference. Diastolic LV inflow and the presence of an accompanying vortex ring were investigated manually for intra‐LV hemodynamics. LV inflow was observed from the left lateral side of the heart. The anterior vortex, generated above the MV and rotating clockwise, and the posterior vortex, generated below the MV and rotating counterclockwise, were identified (Figure 2a, white dashed arrows), and their maximum areas were quantified. The systolic LVOT flow was visualized, and the minimum flow width at the LVOT (Figure 2b, white arrows) and the existence of the LVOT vortex (Figure 2c, white arrowhead) were evaluated. AAO flow patterns were assessed by the presence of a vortex, defined as revolving particles around an axis orthogonal to the vessel centerline, or a helix, defined as a rotational motion around the longitudinal axis of the vessel centerline (Figure 2d, white dashed arrow). The duration and phase counts of the vortex and helix within a cardiac cycle were measured. The existence of an intra‐LA vortex was defined as a rotational flow ≥ 360°, and its area was evaluated (Figure 2e, white dashed arrow). The 4D flow MRI analysis was repeated by an independent second observer (K.O.) to assess interobserver variability.
FIGURE 2.
4D flow MRI images showing the typical flow patterns in HOCM. (a) Diastolic LV anterior vortex above the mitral valve (clockwise rotational arrow) and posterior vortex below (counterclockwise rotational arrow) the mitral valve. (b) Systolic narrowing of the LVOT flow (white arrow). (c) LVOT vortex (white arrowhead). (d) Vortex flow in the ascending aorta (white dashed rotational arrow). (e) Left atrial vortex flow (white rotational arrow). AO, aorta; HOCM, hypertrophic obstructive cardiomyopathy; LA, left atrium; LV, left ventricle; LVOT, left ventricular outflow tract.
2.6. Statistical Analysis
Continuous data are expressed as mean ± standard deviation for normally distributed data or median with interquartile range for nonnormally distributed data. Categorical data are presented as numbers and percentages. The paired t‐test for normally distributed data and Wilcoxon signed–rank test for nonnormally distributed data were used for comparisons before and after ASA. Categorical data were compared using the chi‐squared test or Fisher's exact test, as appropriate. For multiple two‐group comparisons regarding MRI parameters before and after ASA, we controlled the false discovery rate using the Benjamini–Hochberg (BH) procedure (target q = 0.10). We report unadjusted p values and BH‐adjusted q values. Pearson's correlation coefficient (R) was applied to normally distributed parameters, whereas Spearman's correlation coefficient (Rs) was used for non‐normally distributed parameters. The interobserver variabilities for the 4D flow MRI parameters, which were assessed semi‐automatically, including the durations of the vortex and helix in the AAO, LVOT flow width, presence of the LVOT vortex, and vortex sizes in the LV and LA, were evaluated by calculating Cohen's kappa coefficient or intraclass correlation coefficient (ICC). Differences between groups were considered significant if the BH‐adjusted q values were ≤ 0.10. Raw p values are also reported for reference. Correlation coefficients were considered significant when the p value was < 0.05. All statistical analyses were performed using the SPSS software (version 30.0; IBM Corp., Armonk, NY, USA).
3. Results
3.1. Patient Characteristics
Of 38 consecutive patients with HOCM who underwent ASA, all patients underwent baseline cardiac MRI. We excluded five patients with cardiac implantable electronic devices, one with renal dysfunction, and one diagnosed with HOCM after cardiac MRI because they did not undergo 4D flow MRI. Among the remaining 31 patients, five without follow‐up cardiac MRI data and three who received cardiac implantable electronic devices after ASA were excluded. Finally, 23 patients were included in the analysis.
The baseline characteristics, including echocardiographic measurements, are presented in Table 1. The average age was 68.1 ± 8.6 years, and the proportion of male participants was 21.7%. Heart failure symptoms in 30.4% of the patients were classified as New York Heart Association class III or IV. Beta‐blockers, calcium channel antagonists, and sodium channel blockers were used by 18 (78.3%), 12 (52.2%), and 17 (73.9%) patients, respectively. The serum N‐terminal pro‐B‐type natriuretic peptide level was 725.0 (345.0, 1069.0) pg/mL. The resting LVOT peak pressure gradient (PPG) was 102.6 ± 52.9 mmHg, which significantly decreased at follow‐up (24.6 ± 23.1 mmHg). ASA characteristics included the number of ethanol‐injected septal arteries (2.7 ± 1.1), the amount of ethanol used (4.4 ± 1.7 mL), peak creatine kinase (1564.7 ± 556.5 U/L), and the difference in catheter‐based PPG during the procedure (56.5 ± 43.6 mmHg). Follow‐up cardiac MRI was performed 34.1 ± 17.7 months after the ASA.
TABLE 1.
Baseline characteristics.
| Number of patients | n = 23 |
|---|---|
| Age, years | 68.1 ± 8.6 |
| Male sex, n (%) | 5 (21.7) |
| Body mass index, kg/m2 | 23.3 ± 3.8 |
| NYHA class III or IV, n (%) | 7 (30.4) |
| Syncope, n (%) | 6 (26.1) |
| Hypertension, n (%) | 12 (52.2) |
| Diabetes mellitus, n (%) | 2 (8.7) |
| Dyslipidemia, n (%) | 11 (47.8) |
| COPD, n (%) | 1 (4.3) |
| Current smoking, n (%) | 2 (8.7) |
| Stroke, n (%) | 3 (13.0) |
| Atrial fibrillation, n (%) | 4 (17.4) |
| CIED implantation, n (%) | 0 (0.0) |
| Family history of SCD, n (%) | 3 (13.0) |
| Family history of HCM, n (%) | 7 (30.4) |
| Medication | |
| Beta‐blockers, n (%) | 18 (78.3) |
| Calcium channel antagonists, n (%) | 12 (52.2) |
| Sodium channel blockers, n (%) | 17 (73.9) |
| ACE‐Is/ARBs, n (%) | 9 (39.1) |
| Amiodarone, n (%) | 1 (4.3) |
| OACs, n (%) | 5 (21.7) |
| Laboratory data | |
| NT‐pro BNP, pg/mL | 725.0 (345.0, 1069.0) |
| Echocardiographic variables | |
| Max IVST, mm | 16.3 ± 4.1 |
| LAD, mm | 38.0 ± 9.6 |
| LAVI, mL/m2 | 54.9 ± 19.2 |
| Resting LVOT PPG, mmHg | 102.6 ± 52.9 |
| Moderate or severe MR, n (%) | 13 (56.5) |
| Anterior mitral leaflet length, mm | 25.9 ± 4.2 |
| Posterior mitral leaflet length, mm | 16.3 ± 4.4 |
| SAM grade of the mitral valve | |
| G3, n (%) | 13 (56.5) |
| G4, n (%) | 5 (21.7) |
Note: Data are expressed as mean ± standard deviation, median (interquartile range), or number (%).
Abbreviations: ACE‐Is, angiotensin‐converting enzyme inhibitors; ARBs, angiotensin II receptor blockers; CIED, cardiac implantable electronic device; COPD, chronic obstructive pulmonary disease; HCM, hypertrophic cardiomyopathy; LAD, left atrial dimension; LAVI, left atrial volume index; LVOT, left ventricular outflow tract; Max IVST, maximum interventricular septal thickness; MR, mitral regurgitation; NT‐pro BNP, N‐terminal pro‐B‐type natriuretic peptide; NYHA, New York Heart Association; OACs, oral anticoagulants; PPG, peak pressure gradient; SAM, systolic anterior motion; SCD, sudden cardiac death.
3.2. Global Cardiac Volume and LGE
The global cardiac volume and LGE data are summarized in Table 2. LV mass index (LVMI; 80.4 ± 17.5 g/m2 vs. 66.6 ± 14.4 g/m2) and maximum LA volume index (51.0 ± 16.8 mL/m2 vs. 42.4 ± 15.0 mL/m2) significantly decreased after ASA. By contrast, LGE mass (1.06 [0.33, 2.50] vs. 8.99 [5.54, 12.91] g) and %LGE (0.60 [0.26, 2.18]% vs. 7.28 [5.23, 13.78]%) significantly increased after ASA.
TABLE 2.
Cardiac volume, function, and LGE by conventional cardiac MRI before and after ASA.
| Before ASA (n = 23) | After ASA (n = 23) | p | BH q | |
|---|---|---|---|---|
| HR, min | 60.7 ± 8.0 | 63.8 ± 9.2 | 0.071 | 0.187 |
| LVEDVI, mL/m2 | 77.6 ± 14.9 | 76.8 ± 14.3 | 0.593 | 0.903 |
| LVESVI, mL/m2 | 29.5 (22.4, 34.3) | 27.2 (24.2, 31.5) | 0.903 | 0.903 |
| LVSVI, mL/m2 | 48.4 ± 12.0 | 47.9 ± 10.2 | 0.773 | 0.903 |
| LVCI, L/min/m2 | 2.9 ± 0.7 | 3.0 ± 0.7 | 0.539 | 0.903 |
| LVEF, % | 62.1 ± 7.6 | 62.5 ± 7.3 | 0.842 | 0.903 |
| LVMI, g/m2 | 80.4 ± 17.5 | 66.6 ± 14.4 | < 0.001 | < 0.017 |
| RVEDVI, mL/m2 | 60.3 ± 11.4 | 63.6 ± 17.4 | 0.135 | 0.287 |
| RVESVI, mL/m2 | 20.2 (15.3, 26.0) | 20.8 (17.2, 31.1) | 0.121 | 0.187 |
| RVSVI, mL/m2 | 39.2 ± 8.7 | 38.7 ± 9.6 | 0.741 | 0.903 |
| RVCI, L/min/m2 | 2.4 ± 0.7 | 2.4 ± 0.6 | 0.652 | 0.903 |
| RVEF, % | 65.1 ± 8.6 | 61.4 ± 9.1 | 0.048 | 0.163 |
| Min LAVI, mL/m2 | 28.6 ± 13.0 | 25.5 ± 11.9 | 0.203 | 0.383 |
| Max LAVI, mL/m2 | 51.0 ± 16.8 | 42.4 ± 15.0 | < 0.001 | < 0.017 |
| LAEF, % | 43.1 ± 7.5 | 42.8 ± 10.3 | 0.880 | 0.903 |
| LGE mass, g | 1.06 (0.33, 2.50) | 8.99 (5.54, 12.91) | < 0.001 | < 0.017 |
| %LGE, % | 0.60 (0.26, 2.18) | 7.28 (5.23, 13.78) | < 0.001 | < 0.017 |
Note: Data are expressed as mean ± standard deviation or median (interquartile range).
Abbreviations: %LGE, fraction of late gadolinium enhancement to the left ventricular mass; ASA, alcohol septal ablation; BH, Benjamini–Hochberg; HR, heart rate; LAEF, left atrial emptying fraction; LGE, late gadolinium enhancement in the left ventricle; LVCI, left ventricular cardiac index; LVEDVI, left ventricular end‐diastolic volume index; LVEF, left ventricular ejection fraction; LVESVI, left ventricular end‐systolic volume index; LVMI, left ventricular mass index; LVSVI, left ventricular stroke volume index; Max LAVI, maximum left atrial volume index; Min LAVI, minimum left atrial volume index; MRI, magnetic resonance imaging; RVCI, right ventricular cardiac index; RVEDVI, right ventricular end‐diastolic volume index; RVEF, right ventricular ejection fraction; RVESVI, right ventricular end‐systolic volume index; RVSVI, right ventricular stroke volume index.
3.3. Strain and SR
The peak strain and SR are summarized in Table 3. The 2D‐GRS in LAX images increased significantly after ASA (16.5% ± 5.8% vs. 20.1% ± 6.8%), whereas the 2D‐GLS in LAX images decreased significantly after ASA (−10.5% ± 3.2% vs. −12.1% ± 3.5%). The local strains in the 16‐segment model are summarized in Tables S1–S4, and their differences before and after ASA are shown in Figure 3. In the SAX images, the peak radial strain decreased significantly (Table S1 and Figure 3a), and the peak circumferential strain increased significantly (Table S2 and Figure 3b) in the basal anteroseptal segments. In systole, the radial peak SR in LAX images increased significantly [0.82 (0.60, 0.94) vs. 0.87 (0.62, 1.24)/s], and the longitudinal peak SR in LAX images decreased significantly (−0.53 [−0.62, −0.45] vs. −0.59 [−0.77, −0.46]/s). In diastole, the radial peak SR in the LAX images decreased significantly (−0.62 [−0.69, −0.52] vs. −0.73 [−0.88, −0.52]/s).
TABLE 3.
Peak strains in the LV, RV, and LA and peak strain rates in the LV.
| Peak strain | Before ASA (n = 23) | After ASA (n = 23) | p | BH q |
|---|---|---|---|---|
| LV | ||||
| 2D‐GRS in SAX, % | 34.0 ± 7.4 | 34.0 ± 9.2 | 0.968 | 1.000 |
| 2D‐GCS in SAX, % | −18.4 ± 2.9 | −18.3 ± 3.3 | 0.929 | 0.984 |
| 2D‐GRS in LAX, % | 16.5 ± 5.8 | 20.1 ± 6.8 | < 0.001 | < 0.018 |
| 2D‐GLS in LAX, % | −10.5 ± 3.2 | −12.1 ± 3.5 | 0.002 | 0.018 |
| RV | ||||
| 2D‐GRS in SAX, % | 35.5 ± 8.3 | 33.5 ± 5.5 | 0.319 | 0.722 |
| 2D‐GCS in SAX, % | −17.8 ± 3.2 | −17.6 ± 2.1 | 0.794 | 0.948 |
| 2D‐GRS in LAX, % | 45.7 ± 17.9 | 43.8 ± 14.7 | 0.685 | 0.948 |
| 2D‐GLS in LAX, % | −18.3 ± 11.8 | −20.4 ± 4.1 | 0.472 | 0.777 |
| LA | ||||
| Average LAX strain, % | 15.1 ± 7.8 | 13.4 ± 8.0 | 0.314 | 0.722 |
| Average LAX difference, mm | 6.7 ± 3.0 | 6.1 ± 3.0 | 0.361 | 0.722 |
| Peak SR | ||||
| Systole | ||||
| Radial peak SR in SAX/s | 1.40 (1.24, 1.68) | 1.42 (1.24, 1.66) | 0.475 | 0.777 |
| Circumferential peak SR in SAX/s | −0.83 (−0.94, −0.74) | −0.82 (−0.90, −0.75) | 0.831 | 0.948 |
| Radial peak SR in LAX/s | 0.82 (0.60, 0.94) | 0.87 (0.62, 1.24) | 0.006 | 0.036 |
| Longitudinal peak SR in LAX/s | −0.53 (−0.62, −0.45) | −0.59 (−0.77, −0.46) | 0.009 | 0.041 |
| Diastole | ||||
| Radial peak SR in SAX/s | −1.01 (−1.27, −0.76) | −0.91 (−1.38, −0.80) | 0.738 | 0.948 |
| Circumferential peak SR in SAX/s | 0.51 (0.44, 0.57) | 0.53 (0.41, 0.60) | 0.843 | 0.948 |
| Radial peak SR in LAX/s | −0.62 (−0.69, −0.52) | −0.73 (−0.88, −0.52) | 0.039 | 0.140 |
| Longitudinal peak SR in LAX/s | 0.47 (0.36, 0.55) | 0.44 (0.35, 0.59) | 0.345 | 0.722 |
Note: Data are expressed as the mean ± standard deviation or median (interquartile range).
Abbreviations: 2D, two‐dimensional; ASA, alcohol septal ablation; BH, Benjamini–Hochberg; GCS, global circumferential strain; GLS, global longitudinal strain; GRS, global radial strain; LA, left atrium; LAX, long‐axis images; LV, left ventricle; RV, right ventricle; SAX, short‐axis images; SR, strain rate.
FIGURE 3.
Differences in regional 2D peak strains before and after ASA. Regional differences in strain before and after ASA for peak radial strain (a) and peak circumferential strain (b) in the short‐axis image and for peak radial strain (c) and peak longitudinal strain (d) in the long‐axis images are exhibited in the 16‐segment model. Data are expressed as means. * represents statistical significance. ASA, alcohol septal ablation.
3.4. Hemodynamics by 4D Flow MRI
Diastolic LV anterior vortex area increased significantly after ASA (2256.1 [703.6, 4038.4] vs. 3826.1 [1914.3, 4820.1] mm2; Table 4). The systolic LVOT flow width widened after ASA (7.28 ± 3.45 mm vs. 10.17 ± 3.44 mm), and the LVOT vortex decreased after ASA (16 [69.6%] vs. 4 [17.4%]). The prevalence of the AAO vortex or helix before ASA did not change after ASA (23 [100%] vs. 23 [100%], p > 0.999). However, the duration of the vortex or helix significantly decreased after ASA (in phase count: 12.1 ± 4.5 phases vs. 10.7 ± 4.5 phases; 538.8 ± 222.4 ms vs. 454.8 ± 181.9 ms). The interobserver variabilities for the 4D flow MRI parameters were as follows: diastolic LV vortex area (ICC = 0.95), systolic LVOT flow width (ICC = 0.93), prevalence of the systolic LVOT vortex (kappa = 0.68), prevalence of the AAO vortex and helix (kappa = 0.80), and duration of the AAO vortex or helix (ICC = 0.93).
TABLE 4.
4D flow MRI before and after ASA.
| Before ASA (n = 23) | After ASA (n = 23) | p | BH q | |
|---|---|---|---|---|
| LV | ||||
| Diastolic LV anterior vortex area, mm2 | 2256.1 (703.6, 4038.4) | 3826.1 (1914.3, 4820.1) | 0.036 | 0.079 |
| Diastolic LV posterior vortex area, mm2 | 803.3 (585.6, 1358.7) | 884.4 (730.5, 1356.8) | 0.808 | 1.000 |
| Systolic LVOT flow width, mm | 7.28 ± 3.45 | 10.17 ± 3.44 | < 0.001 | < 0.011 |
| Systolic LVOT vortex, n (%) | 16 (69.6) | 4 (17.4) | < 0.001 | < 0.011 |
| AAO | ||||
| Vortex, n (%) | 20 (87.0) | 19 (82.6) | > 0.999 | 1.000 |
| Helix, n (%) | 15 (65.2) | 15 (65.2) | > 0.999 | 1.000 |
| Vortex or helix, n (%) | 23 (100) | 23 (100) | > 0.999 | 1.000 |
| V/H duration, phase | 12.1 ± 4.5 | 10.7 ± 4.5 | 0.007 | 0.019 |
| V/H duration, ms | 538.8 ± 222.4 | 454.8 ± 181.9 | 0.005 | 0.018 |
| LA | ||||
| Vortex, n (%) | 17 (72.7) | 15 (68.2) | 0.749 | 1.000 |
| Vortex area, mm2 | 4051.8 ± 1598.9 | 4205.8 ± 2465.5 | 0.717 | 1.000 |
Note: Data are expressed as the mean ± standard deviation, median (interquartile range), or number (%).
Abbreviations: 4D, four‐dimensional; AAO, ascending aorta; ASA, alcohol septal ablation; BH, Benjamini–Hochberg; LA, left atrium; LV, left ventricular; LVOT, left ventricular outflow tract; MRI, magnetic resonance imaging; V/H, vortex or helix.
3.4.1. Successful ASA and Cardiac MRI Findings Before and After ASA
Post‐procedural evaluation revealed that four patients (17.4%) had a persistent resting LVOT PPG > 50 mmHg, indicating incomplete myocardial ablation. Demographic data and cardiac MRI parameters comparing patients with successful ASA (responders, n = 19) and unsuccessful ASA (non‐responders, n = 4) are summarized in Table S5. On cardiac MRI before ASA, responder exhibited larger LVESVI (30.1 ± 6.4 mL/m2 vs. 21.4 ± 1.7 mL/m2), lower LVEF (60.5% ± 7.4% vs. 69.7% ± 2.5%), reduced LV peak strains (GRS in SAX, 32.33% ± 6.68% vs. 41.79% ± 6.26%; GCS in SAX, −17.73% ± 2.61% vs. −21.54% ± 1.87%; GRS in LAX, 15.24% ± 4.86% vs. 22.3% ± 6.76%; GLS in LAX, −9.86% ± 2.85% vs. −13.72% ± 3.24%), reduced LV peak SRs in both systole (radial peak SR in LAX, 0.67 [0.57, 0.91] vs. 1.01 [0.85, 1.33]/s; longitudinal peak SR in LAX, −0.48 [−0.61, −0.43] vs. −0.65 [−0.85, −0.56]/s) and diastole (radial peak SR in LAX, −0.55 [−0.65, −0.48] vs. −0.82 [−0.97, −0.71]/s; longitudinal peak SR in LAX, 0.38 [0.36, 0.51] vs. 0.56 [0.53, 0.63]/s) compared with non‐responder. On cardiac MRI after ASA, responders showed lower RVEF (59.4% ± 8.7% vs. 70.9% ± 3.8%), reduced diastolic circumferential peak SR in SAX (0.47 [0.38, 0.55] vs. 0.68 [0.61, 0.73]), and reduced diastolic radial peak SR in LAX (−0.65 [−0.81, −0.5]) compared to those in non‐responder.
3.5. Associations Among Cardiac Volume, Strain, Hemodynamics, and Combined Measurements
The maximum LA volume index was significantly lower in patients with LA vortex than in those without LA vortex (48.71 ± 13.08 mL/m2 vs. 63.19 ± 19.96 mL/m2). LVMI was significantly correlated with LV 2D‐GRS and 2D‐GCS in the SAX images, as well as with LV 2D‐GRS and 2D‐GLS in the LAX images (Figure 4a–d). Systolic LVOT flow width was significantly correlated with LV 2D‐GRS and 2D‐GLS in the LAX image (Figure 4e,f). The diastolic LV anterior vortex area was not significantly correlated with the global peak strains or global SRs in diastole or systole (Figures S1 and S2). In contrast, the multiplication of LV end‐diastolic volume index (LVEDVI) × GCS in SAX images × diastolic radial peak SR in LAX images revealed a significant correlation with the diastolic LV anterior vortex area before ASA (Rs = 0.43; Figure 5a). The multiplication index of three parameters (LVEDVI × GCS in SAX images × diastolic radial peak SR in LAX images) increased significantly after ASA (8.87 ± 3.58 mL/m2/s vs. 10.29 ± 4.87 mL/m2/s) and there was no significant correlation with diastolic LV anterior vortex area (Rs = 0.38, p = 0.072; Figure 5b).
FIGURE 4.
Correlations between LVMI and LV 2D strain parameters, and between LVOT flow width and LV 2D strain parameters. Scatter plots showing the significant correlation between LVMI and LV 2D‐GRS (a), LVMI and LV 2D‐GCS (b) in the short‐axis images, LVMI and LV 2D‐GRS (c) and LVMI and LV 2D‐GLS (d) in the long‐axis images, systolic LVOT flow width and LV 2D‐GRS (e) and systolic LVOT flow width and LV 2D‐GLS (f) in the long‐axis images. ASA, alcohol septal ablation; GCS, global circumferential strain; GLS, global longitudinal strain; GRS, global radial strain; LV, left ventricular; LVMI, left ventricular mass index; LVOT, left ventricular outflow tract.
FIGURE 5.
Correlations between the diastolic vortex area and the combined multiplication parameters of LVEDVI, the GCS on the SAX images, and the diastolic radial peak SR on the LAX images. Scatter plots showing the relationship between the diastolic LV anterior vortex area and multiplication of three parameters (LVEDVI × GCS in SAX images × diastolic radial peak SR in LAX images) before ASA (a) and after ASA (b). ASA, alcohol septal ablation; GCS, global circumferential strain; LAX, long axis; LV, left ventricle; LVEDVI, left ventricular end‐diastolic volume index; PSR, peak strain rate; SAX, short axis; SR, strain rate.
4. Discussion
This study investigated cardiac deformation and hemodynamic changes at long‐term follow‐up after ASA. FT MRI revealed improved GRS, GLS, and SR in systole and diastole; 4D flow MRI revealed an enlarged diastolic LV vortex, ameliorated LVOT and AAO flow with widened systolic LVOT flow, a reduced LVOT vortex, and a weakened AAO vortex. Finally, the associations of the diastolic LV vortex with LV size and function including strain and SR were demonstrated.
LGE mass increase and LV mass index reduction might directly result from ASA, consistent with the findings of Duan et al. [19]. In contrast to the persistence of LVMI observed when comparing baseline with 1 week after ASA [13], Nagueh et al. [20] reported that, 6 weeks after ASA for HOCM, LV hypertrophy was attenuated, with histological evidence of reduced myocyte size and amount of interstitial collagen. Similarly, Luo et al. [21] demonstrated that septal myectomy decreased LVMI, myocardial cellular and extracellular compartment measured using cardiac MRI. These observations indicate that septal reduction therapy induces regression of LVMI, which includes both cellular and extracellular matrix in remote myocardium. In this context, the improvement of strain in remote myocardium observed in our strain analysis appears in line with these findings. Consistent with prior studies of echocardiography [22, 23], computed tomography [24], and MRI [19] analysis revealed a reduction in the maximum LA volume index, suggesting a reduction in LV end‐diastolic pressure (LVEDP) due to a reduced LVOT pressure gradient. This study did not observe an increase in LVEDVI after ASA. However, previous reports on changes in LV end‐diastolic size after septal reduction therapy are inconsistent, with some reporting an enlargement [22, 25] and others reporting no change [26, 27]. The impact of ASA on LV end‐diastolic size is thought to involve two components: decreased LVEDP, resulting in a decreased LV end‐diastolic size, and alleviating hypercontraction, leading to myocardial relaxation concomitant with an increased LV end‐diastolic size. In this study, the former and the latter may have offset each other.
Regional peak strain was impaired in the basal anteroseptal segment, where the myocardium was ablated by the intervention, whereas that in the remote myocardium generally improved after ASA. Consistent with our findings, van Dockum et al. [28] demonstrated an improved local shortening index in the remote myocardium after ASA via the MRI tissue tagging technique. The increased GRS and GLS in LAX images may have resulted from improved LV contraction associated with reduced LVEDP. However, the GRS and GCS in the SAX images did not significantly increase after ASA. These inconsistencies may be due to heterogeneity in local changes in strain mentioned above. Specifically, the significant deterioration of local strain in the basal anteroseptal segments caused by direct myocardial injury by ASA was more prominent in the SAX images, potentially masking the increased global strain in the SAX images. In contrast, the anteroseptal segments were not fully covered in the 2‐chamber, 3‐chamber, or 4‐chamber LAX images, indicating improved strain in the remote segments. Another intervention involving treatment with metoprolol, which reduced heart rate and increased LV preload, also revealed improved LV GLS [29]. In contrast, a study using speckle‐tracking echocardiography in patients with HOCM undergoing septal reduction therapy via myectomy reported deteriorated LV GLS after the intervention [30]. The potential reason for these contrasting results in the latter study might be due to the adverse effects of the surgical procedure. The significant increase in systolic and diastolic peak SRs in the current study aligned with the findings of a previous study in which speckle‐tracking echocardiography was used [23]. In summary, these results suggest improved systolic and diastolic function after ASA.
The changes in hemodynamics in the LV and AAO before ASA and in the long‐term follow‐up after ASA were similar to those reported in a previous study conducted before and 1 week after ASA [13]. The prevalence of the LA vortex was associated with a smaller maximum LA volume index, which seems to be similar to the association between LA vortex formation and LA size reported in a previous study [31]. The correlation between the diastolic LV vortex area and the multiplication index of the LVEDVI × GCS × diastolic peak SR suggests that the formation of the diastolic LV vortex is supported by each component of the multiplication index, that is, a larger LV cavity and better systolic and diastolic function. A prior 4D flow MRI study [8], which revealed a larger LV vortex in the enlarged LV, supports the association between the LV vortex size and the LV volume observed in the current study.
The diastolic LV vortex flow might be generated on and under the MV, where the inflow directions and the adjacent wall separate, resulting in vortex ring formation [32]. This observation suggests that patients with HOCM are less likely to generate a large vortex flow in the LV because the longer mitral leaflet approaches the ventricular wall, preventing the flow separation. Considering the correlation between the diastolic LV vortex size and the LVEDVI and diastolic SR, a small LV cavity and decreased diastolic SR may suppress the generation of an LV vortex. This association suggests that the diastolic LV anterior vortex may open the LVOT in early systole by pressing down the mitral anterior leaflet. Thus, the diastolic LV anterior vortex may control SAM generation or suppression. In contrast, because ASA reduces the basal anteroseptal wall thickness and suppresses motion, an increased LVOT cavity may promote vortex expansion and suppress SAM.
4.1. Limitations
It was a single‐center, single vendor, single field strength, retrospective observational study with a small sample size, which may have caused patient selection bias. In addition, due to the limited sample size, we were unable to perform multivariable analyses adjusting for clinical characteristics, which should be addressed in future studies with larger cohorts. The absence of a control group was also a limitation of the study. A considerable proportion of patients were excluded due to contraindications such as cardiac implantable electronic device, as well as being followed up at hospitals other than the ASA treatment center, limiting the availability of MRI. Imaging was performed at 3T, and whereas major findings are expected to persist, minor differences in measurement precision may occur at 1.5T scanners commonly used in clinical practice. The high VENC setting used to capture extreme outflow velocities may have limited the resolution of slower intracardiac flow. However, repeated examinations of deformation and hemodynamics using cardiac MRI could provide details on HOCM pathophysiology in patients undergoing ASA.
5. Conclusions
FT and 4D flow MRI revealed improved systolic and diastolic LV function after ASA. Comprehensive cardiac MRI, which provides strain‐related parameters and hemodynamics, could benefit the evaluation of patients with HOCM undergoing ASA. The simplification of 4D flow MRI analysis processes and a large‐scale prospective follow‐up study investigating the associations among hemodynamic variables and prognostic outcomes are warranted to enhance the clinical value of hemodynamic assessment.
Author Contributions
K.S. was involved in the conceptualization, methodology, investigation, formal analysis, writing of the original draft, visualization, and funding acquisition. K.O. was involved in the data validation and manuscript editing. T.S., R.S., and K.I. were involved in the investigation and manuscript editing. Y.M. was involved in the conceptualization, supervision, and manuscript editing.
Consent
All patients provided written informed consent.
Conflicts of Interest
Y.M. reports the receipt of scholarship funds or donation scholarship funds from Abbott Medical Japan LLC and BIOTRONIK JAPAN. The other authors declare no conflicts of interest.
Supporting information
Figure S1: Associations between the diastolic vortex area and strain. Scatter plot showing the relationships between the diastolic left ventricle (LV) anterior vortex area and global radial strain (GRS) (a) and global circumferential strain (GCS) (b) in short‐axis (SAX) images and between the GRS (c) and global longitudinal strain (GLS) (d) in long‐axis (LAX) images.
Figure S2: Associations between diastolic vortex area and diastolic strain rates. Scatter plot showing the relationships between diastolic left ventricle (LV) anterior vortex area and diastolic peak radial strain rate (SR) (a) and diastolic peak circumferential SR (b) in short‐axis (SAX) images and diastolic peak radial SR (c) and diastolic peak longitudinal SR (d) in long‐axis (LAX) images.
Table S1: Regional radial two‐dimensional peak strain via short‐axis images in the American Heart Association 16‐segment model.
Table S2: Regional circumferential two‐dimensional peak strain via short‐axis images in the American Heart Association 16‐segment model.
Table S3: Regional radial two‐dimensional peak strain via long‐axis images in the American Heart Association 16‐segment model.
Table S4: Regional longitudinal two‐dimensional peak strain via long‐axis images in the American Heart Association 16‐segment model.
Table S5: Demographics and cardiac MRI findings in ASA responders versus non‐responders.
Acknowledgments
The authors have nothing to report.
Suwa K., Ohno K., Satoh T., Sato R., Iguchi K., and Maekawa Y., “Alcohol Septal Ablation in Hypertrophic Obstructive Cardiomyopathy: Long‐Term Follow‐Up of Deformations and Hemodynamics,” Journal of Magnetic Resonance Imaging 63, no. 3 (2026): 859–871, 10.1002/jmri.70156.
Funding: This study received funding from the Ministry of Education, Culture, Science, Sports and Technology of Japan, Grants‐in‐Aid for Scientific Research (grant number: 20K17144 to K.S.) and HUSM Grant‐in‐Aid for data analysis and manuscript preparation.
Data Availability Statement
The data underlying this article will be shared upon reasonable request to the corresponding author.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Figure S1: Associations between the diastolic vortex area and strain. Scatter plot showing the relationships between the diastolic left ventricle (LV) anterior vortex area and global radial strain (GRS) (a) and global circumferential strain (GCS) (b) in short‐axis (SAX) images and between the GRS (c) and global longitudinal strain (GLS) (d) in long‐axis (LAX) images.
Figure S2: Associations between diastolic vortex area and diastolic strain rates. Scatter plot showing the relationships between diastolic left ventricle (LV) anterior vortex area and diastolic peak radial strain rate (SR) (a) and diastolic peak circumferential SR (b) in short‐axis (SAX) images and diastolic peak radial SR (c) and diastolic peak longitudinal SR (d) in long‐axis (LAX) images.
Table S1: Regional radial two‐dimensional peak strain via short‐axis images in the American Heart Association 16‐segment model.
Table S2: Regional circumferential two‐dimensional peak strain via short‐axis images in the American Heart Association 16‐segment model.
Table S3: Regional radial two‐dimensional peak strain via long‐axis images in the American Heart Association 16‐segment model.
Table S4: Regional longitudinal two‐dimensional peak strain via long‐axis images in the American Heart Association 16‐segment model.
Table S5: Demographics and cardiac MRI findings in ASA responders versus non‐responders.
Data Availability Statement
The data underlying this article will be shared upon reasonable request to the corresponding author.