Ultrasound study of layer-specific strain and perfusion of left ventricular myocardium in patients with dilated cardiomyopathy

Purpose To investigate the changes in deformation and myocardial microcirculation perfusion of left ventricular three-layer myocardium in patients with dilated cardiomyopathy (DCM) by using speckle tracking imaging (STI) and myocardial contrast echocardiography (MCE). Methods Twenty-four patients with DCM and 19 healthy controls were selected. Two-dimensional and MCE dynamic images of apical four-chamber, two-chamber, and three-chamber sections and left ventricular mitral valve, papillary muscle and apex sections were collected. The peak values of longitudinal strain (LS), circumferential strain (CS), cross-sectional area of a microvessel (A) and average myocardial microvascular lesion (β) were obtained by Qlab 10.8 workstation values, and myocardial blood flow (MBF) was calculated with A × β to evaluate the deformation and coronary microvascular perfusion of left ventricular three-layer myocardium. Results The brain natriuretic peptide (BNP), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVEDS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left atrial volume index (LAVI), E peak in early diastolic period/A peak velocity in late diastolic period (E/A) and average E/e' in the DCM group were higher than those in the control group (P < 0.05); left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS) rate, stroke volume (SV), cardiac output (CO), cardiac index (CI), A peak, and the e' and a' velocities of both the lateral wall and interventricular septum were smaller than those in the control group (P < 0.05). The LS, CS, A, β, and A × β of the DCM group were all lower than those of the control group, The time to peak and the cardiac cycle required to reach the peak were longer than those in the control group (P < 0.05). The pattern of myocardial strain and perfusion among myocardial layers was subendocardial > middle > subepicardial. The correlation coefficients of LS with A, β, and A × β were − 0.500, -0.279 and − 0.190, respectively, and the correlation coefficients of CS with A, β, and A × β were − 0.383, -0.255 and − 0.208, respectively. Conclusions The deformation of the three-layer myocardium and coronary microcirculation perfusion in DCM patients were diffusely damaged from the endocardium to the epicardium, layer by layer. The longitudinal function of the left ventricular myocardium was closely related to changes in myocardial microcirculation perfusion. Echocardiography is helpful to evaluate myocardial blood flow and myocardial ischemia in patients with DCM.

Study on the Relationship Between Myocardial Microcirculation Perfusion and Electrocardiogram ST Segment Depression in Patients With Hypertrophic Cardiomyopathy

Objective: To investigate the correlation between myocardial microcirculation perfusion status and the ST-segment depression(STD) in patients with hypertrophic cardiomyopathy (HCM)Method: Myocardial microcirculation perfusion of 32 patients with HCM (HCM group) and 28 healthy volunteers (control group) were examined using MCE, and the parameters including peak intensity (PI), area under the curve (AUC), rising slope (RS), and the time to peak (TTP) were analyzed. All subjects were examined by electrocardiogram, and the amplitude of downward movement of ST segment was measured. Then patients were divided into 3 groups according to the degree of downward movement of ST segment: ST1 group (0<ST≤0.1 MV); ST2 group (0.1 MV<ST≤0.2MV); ST3 group (0.2< MV<ST≤0.3 MV). At last, the relationship between myocardial microcirculation disorder and the degree of ST segment depression was explored.Results: Patents with HCM exhibit lower PI and AUC than their healthy counterparts (P < 0.001). No significant difference was found in RS and TTP between two groups (P > 0.05). ST depression was found in all the patients in the HCM group (P < 0.001). There was no significant linear correlation between PI and the degree of ST segment depression (r = -0.348). Then PI value was compared among ST1, ST2, ST3 and control group. The results showed that the PI value in both ST1 group and ST2 group differs from ST3 group (P < 0.01), while there was no significant difference between ST1 and ST2 group (P < 0.05). Conclusion: When ST depressed more than 0.20 mV, the STD is related to the decrease of microcirculation perfusion in hypertrophic myocardium.

Intracoronary Thrombolysis in Patients With ST-Segment Elevation Myocardial Infarction: A Meta-Analysis of Randomized Controlled Trials

Background: The effects of intracoronary (IC) thrombolysis therapy in patients with ST-segment elevation myocardial infarction (STEMI) receiving primary percutaneous coronary intervention (PPCI) remain unclear. Methods: The meta-analysis was conducted according to the PRISMA statement. All relevant studies were identified by searching the PubMed, EMBASE, Cochrane Library, and Web of Science, with no time or language limitation. The pooled risk ratio (RR) and weighted mean difference (WMD) with a 95% CI were calculated. Results: Nine randomized controlled trials involving a total of 1341 patients were included. Compared with the control group, IC thrombolysis in patients with STEMI could reduce the incidence of major adverse cardiac events (MACE; RR 0.632, 95% CI, 0.474-0.843, P = .002) and improve left ventricular ejection fraction (RR 0.343, 95% CI, 0.178-0.509, P < .001) and myocardial microcirculation. However, there was no difference noted in the mortality (RR 0.759, 95% CI, 0.347-1.661, P = .490). The incidence rate of major bleeding and minor bleeding was comparable between the 2 groups. Conclusions: Intracoronary thrombolysis was associated with improved MACE and myocardial microcirculation in patients with STEMI having PPCI, though it failed to improve mortality.

Ultrasound Study of Layer-specific Strain and Perfusion of Left Ventricular Myocardium in Patients With Dilated Cardiomyopathy

BackgroundTo investigate the changes in deformation and myocardial microcirculation perfusion of left ventricular three-layer myocardium in patients with dilated cardiomyopathy (DCM) by using speckle tracking imaging (STI) and myocardial contrast echocardiography (MCE).MethodsTwenty-four patients with DCM and 19 healthy controls were selected. Two-dimensional and MCE dynamic images of apical four-chamber, two-chamber, and three-chamber sections and left ventricular mitral valve, papillary muscle and apex sections were collected. The peak values of longitudinal strain (LS), circumferential strain (CS), cross-sectional area of a microvessel (A) and average myocardial microvascular lesion (β) were obtained by Qlab 10.8 workstation values, and myocardial blood flow (MBF) was calculated with A×β to evaluate the deformation and coronary microvascular perfusion of left ventricular three-layer myocardium.ResultsThe brain natriuretic peptide (BNP), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVEDS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left atrial volume index (LAVI), E peak in early diastolic period/A peak velocity in late diastolic period (E/A) and average E/e' in the DCM group were higher than those in the control group (P < 0.05); left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS) rate, stroke volume (SV), cardiac output (CO), cardiac index (CI), A peak, and the e' and a' velocities of both the lateral wall and interventricular septum were smaller than those in the control group (P<0.05). The LS, CS, A, β, and A×β of the DCM group were all lower than those of the control group (P < 0.05). The pattern of myocardial strain and perfusion among myocardial layers was subendocardial>middle>subepicardial. The correlation coefficients of LS with A, β, and A×β were -0.500, -0.279 and -0.190, respectively, and the correlation coefficients of CS with A, β, and A×β were -0.383, -0.255 and -0.208, respectively.ConclusionsThe deformation of the three-layer myocardium and coronary microcirculation perfusion in DCM patients were diffusely damaged from the endocardium to the epicardium, layer by layer. The longitudinal function of the left ventricular myocardium was closely related to changes in myocardial microcirculation perfusion.

Ultrasound Study of Layer-specific Strain and Perfusion of Left Ventricular Myocardium in Patients With Dilated Cardiomyopathy

BackgroundTo investigate the changes in deformation and myocardial microcirculation perfusion of left ventricular three-layer myocardium in patients with dilated cardiomyopathy (DCM) by using speckle tracking imaging (STI) and myocardial contrast echocardiography (MCE).MethodsTwenty-four patients with DCM and 19 healthy controls were selected. Two-dimensional and MCE dynamic images of apical four-chamber, two-chamber, and three-chamber sections and left ventricular mitral valve, papillary muscle and apex sections were collected. The peak values of longitudinal strain (LS), circumferential strain (CS), cross-sectional area of a microvessel (A) and average myocardial microvascular lesion (β) were obtained by Qlab 10.8 workstation values, and myocardial blood flow (MBF) was calculated with A×β to evaluate the deformation and coronary microvascular perfusion of left ventricular three-layer myocardium.ResultsThe brain natriuretic peptide (BNP), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVEDS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left atrial volume index (LAVI), E peak in early diastolic period/A peak velocity in late diastolic period (E/A) and average E/e' in the DCM group were higher than those in the control group (P < 0.05); left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS) rate, stroke volume (SV), cardiac output (CO), cardiac index (CI), A peak, and the e' and a' velocities of both the lateral wall and interventricular septum were smaller than those in the control group (P<0.05). The LS, CS, A, β, and A×β of the DCM group were all lower than those of the control group (P < 0.05). The pattern of myocardial strain and perfusion among myocardial layers was subendocardial>middle>subepicardial. The correlation coefficients of LS with A, β, and A×β were -0.500, -0.279 and -0.190, respectively, and the correlation coefficients of CS with A, β, and A×β were -0.383, -0.255 and -0.208, respectively.ConclusionsThe deformation of the three-layer myocardium and coronary microcirculation perfusion in DCM patients were diffusely damaged from the endocardium to the epicardium, layer by layer. The longitudinal function of the left ventricular myocardium was closely related to changes in myocardial microcirculation perfusion.

Ultrasound Study of Layer-specific Strain and Perfusion of Left Ventricular Myocardium in Patients With Dilated Cardiomyopathy

BackgroundTo investigate the changes in deformation and myocardial microcirculation perfusion of left ventricular three-layer myocardium in patients with dilated cardiomyopathy (DCM) by using speckle tracking imaging (STI) and myocardial contrast echocardiography (MCE).MethodsTwenty-four patients with DCM and 19 healthy controls were selected. Two-dimensional and MCE dynamic images of apical four-chamber, two-chamber, and three-chamber sections and left ventricular mitral valve, papillary muscle and apex sections were collected. The peak values of longitudinal strain (LS), circumferential strain (CS), cross-sectional area of a microvessel (A) and average myocardial microvascular lesion (β) were obtained by Qlab 10.8 workstation values, and myocardial blood flow (MBF) was calculated with A×β to evaluate the deformation and coronary microvascular perfusion of left ventricular three-layer myocardium.ResultsThe brain natriuretic peptide (BNP), left ventricular mass index (LVMI), left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVEDS), left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left atrial volume index (LAVI), E peak in early diastolic period/A peak velocity in late diastolic period (E/A) and average E/e' in the DCM group were higher than those in the control group (P < 0.05); left ventricular ejection fraction (LVEF), left ventricular fractional shortening (FS) rate, stroke volume (SV), cardiac output (CO), cardiac index (CI), A peak, and the e' and a' velocities of both the lateral wall and interventricular septum were smaller than those in the control group (P<0.05). The LS, CS, A, β, and A×β of the DCM group were all lower than those of the control group (P < 0.05). The pattern of myocardial strain and perfusion among myocardial layers was subendocardial>middle>subepicardial. The correlation coefficients of LS with A, β, and A×β were -0.500, -0.279 and -0.190, respectively, and the correlation coefficients of CS with A, β, and A×β were -0.383, -0.255 and -0.208, respectively.ConclusionsThe deformation of the three-layer myocardium and coronary microcirculation perfusion in DCM patients were diffusely damaged from the endocardium to the epicardium, layer by layer. The longitudinal function of the left ventricular myocardium was closely related to changes in myocardial microcirculation perfusion.

Impaired perfusion in the myocardial microcirculation in asymptomatic patients with Stages 1–4 chronic kidney disease with intrarenal arterial lesions

Background Even mild renal disease is a powerful cardiovascular risk factor. However, the association between these pathophysiologic processes (especially in the early asymptomatic stage) is not known. Methods We recruited 243 asymptomatic patients with Stages 1–4 chronic kidney disease (CKD) without obstructive coronary artery disease (CAD). We distinguished different degrees of severity of intrarenal arterial lesions (IALs) according to the Oxford classification. Myocardial microcirculation perfusion was measured using single-photon emission computed tomography (SPECT). Summed scores of 17 stress and rest image segments produced the summed stress score (SSS) and summed rest score (SRS), respectively. The summed difference score (SDS) was calculated as the difference between the SSS and SRS. Coronary microvascular disease (CMD) was defined as abnormal SPECT (SSS ≥4 or SDS ≥2) in the absence of obstructive CAD. Results Participants showed a stepwise increase in CMD severity with IAL aggravation. SSS of no/mild/moderate/severe IALs was 1.64 ± 1.08, 2.56 ± 1.35, 4.42 ± 2.17 and 6.48 ± 3.52, respectively (P &lt; 0.05 for all). SDS of no/mild/moderate/severe IALs was 1.29 ± 0.49, 1.75 ± 0.56, 3.06 ± 1.12 and 4.16 ± 1.85, respectively (P &lt; 0.05 for all). The percentage of subclinical CMD in CKD patients with IALs was significantly higher than in those without IALs (69.57% versus 14.71%; P = 0.01). Multiple regression analysis showed that renal arteriolar hyalinization (odds ratio = 1.578, P = 0.009) was associated independently with subclinical CMD. Conclusions We demonstrated, for the first time, that impaired perfusion in the myocardial microcirculation in asymptomatic patients with Stages 1–4 CKD with IALs. Renal arteriolar hyalinization may be a useful marker of CMD in CKD.

P0702IMPAIRED MYOCARDIAL MICROCIRCULATION PERFUSION IN ASYMPTOMATIC STAGE 1-4 CHRONIC KIDNEY DISEASE PATIENTS WITH INTRARENAL ARTERIAL LESIONS

Background and Aims Even mild renal disease is a powerful cardiovascular (CV) risk factor. However, the association between these pathophysiological processes, especially in the early asymptomatic stage, remains unclear. This study aimed to explore the relationship of cardio-renal microvascular disease in asymptomatic stage 1-4 chronic kidney disease (CKD) patients without obstructive coronary artery disease (CAD). Method This study consisted of 243 asymptomatic patients with stage 1-4 CKD who had no obstructive CAD. We distinguished different degrees of severity of intrarenal arterial lesions according to Oxford classification. Myocardial microcirculation perfusion was measured using single-photon emission computed tomography (SPECT). The summed stress score (SSS), summed rest score (SRS), and summed difference score (SDS) were estimated with the standard 17-segment, 5-point scoring model. Coronary microvascular disease (CMD) was defined as abnormal SPECT MPI (SSS ≥4 or SDS≥2 on SPECT images) in the absence of obstructive CAD. Results The study subjects showed a stepwise increase in CMD severity with the aggravation of intrarenal arterial lesions; The SSS of no/mild/moderate/severe arterial lesions were 1.64±1.08, 2.56±1.35, 4.42±2.17, 6.48±3.52, respectively (all P&lt;0.05); The SDS of no/mild/moderate/severe arterial lesions were 1.29±0.49, 1.75±0.56, 3.06±1.12, 4.16±1.85, respectively (all P&lt;0.05). The percentage of subclinical CMD in CKD patients with intrarenal arterial lesions was significantly higher than those without arterial lesions (69.57% vs. 14.71%; P=0.01). Vice versa, the scores of intrarenal arterial lesions were significantly higher in patients who had myocardial perfusion defect (4.79±2.01 vs. 2.22±2.07, P=0.000), myocardial ischemia (3.69±2.16 vs. 2.35±1.69, P=0.001) compared to those without arterial lesions. Multiple regression analysis further supported renal arterioles hyalinization (OR=1.109, P=0.027) were independently associated with subclinical CMD in stage 1-4 CKD patients with no obstructive CAD. Conclusion This study demonstrated for the first time impaired myocardial microcirculation perfusion in asymptomatic stage 1-4 CKD patients with intrarenal arterial lesions. Renal arteriolar hyalinization may be a useful marker of the presence of CMD in CKD.