Traditionally, individuals with hypertrophic cardiomyopathy (HCM) have been advised not to participate in more than low-intensity exercises. HCM was originally described in the context of sudden ...death, and early literature from the registry showed that HCM was the most common cause of sudden cardiac death in young athletes. Therefore, there has long been a concern that exercise could trigger ventricular arrhythmia and sudden cardiac death. Although a few patients with HCM may progress along deteriorating disease pathways, many have no clinically significant symptoms or adverse events, no need for major treatment, and a normal life expectancy. Therefore, the routine restriction of any exercise intensity in this large group deprives them of the multiple benefits of exercise and may have detrimental effects on long-term clinical outcomes. However, it has been reported that light to moderate exercise is acceptable for many patients with HCM, and recent evidence suggests that vigorous exercise does not increase the risk of sudden death in this population. Thus, we reviewed previous literature regarding the effects of exercise in patients with HCM and provided cutting-edge information on the safety and concerns of exercise. In addition, based on our experience and previous research, we reviewed the conditions that should be met before starting exercise and the tests required to confirm them.Traditionally, individuals with hypertrophic cardiomyopathy (HCM) have been advised not to participate in more than low-intensity exercises. HCM was originally described in the context of sudden death, and early literature from the registry showed that HCM was the most common cause of sudden cardiac death in young athletes. Therefore, there has long been a concern that exercise could trigger ventricular arrhythmia and sudden cardiac death. Although a few patients with HCM may progress along deteriorating disease pathways, many have no clinically significant symptoms or adverse events, no need for major treatment, and a normal life expectancy. Therefore, the routine restriction of any exercise intensity in this large group deprives them of the multiple benefits of exercise and may have detrimental effects on long-term clinical outcomes. However, it has been reported that light to moderate exercise is acceptable for many patients with HCM, and recent evidence suggests that vigorous exercise does not increase the risk of sudden death in this population. Thus, we reviewed previous literature regarding the effects of exercise in patients with HCM and provided cutting-edge information on the safety and concerns of exercise. In addition, based on our experience and previous research, we reviewed the conditions that should be met before starting exercise and the tests required to confirm them.
Some patients exhibit discrepancies in carotid and coronary artery atherosclerosis. This study aimed to define the characteristics and prognosis of these discrepant patients and determine the best ...strategy to detect pan-vascular atherosclerosis. A database of 5,022 consecutively registered patients who underwent both coronary angiography and carotid ultrasonography, along with clinical and blood laboratory tests, echocardiography, and pulse wave velocity (PWV), was analyzed. The development of cerebro-cardiovascular (CV) events during the follow-up period was also evaluated. A significant proportion of patients (n = 1,741, 35%) presented with a discrepancy between carotid artery plaque and coronary artery disease (CAD). In patients without carotid plaque, male sex (odds ratio OR, 1.71; 95% confidence interval CI, 1.20-2.41; P = 0.003), older age (OR, 1.03; 95% CI, 1.01-1.04; P = 0.002), smoking history (OR, 1.58; 95% CI, 1.13-2.20; P = 0.008), lower high-density lipoprotein (HDL) -cholesterol level (OR, 0.97; 95% CI, 0.96-0.98; P < 0.001), and lower common carotid artery end-diastolic velocity (CCA-EDV) (OR, 0.97; 95% CI, 0.95-0.99; P = 0.005) were independently related to the presence of CAD. In patients without CAD, increased PWV was independently related to the presence of carotid plaque. In survival analysis, patients with isolated CAD had a higher probability of composite CV events; those with isolated carotid plaque had a higher probability of heart failure (HF) and mortality than their counterpart groups (P < 0.05). Even in patients without carotid artery plaque, careful coronary evaluation is needed in older or male patients with smoking history, lower HDL-cholesterol level, or lower CCA-EDV. Carotid plaque may be a potential risk factor for HF.
Aims
Increased red cell distribution width (RDW) is a poor prognostic factor in patients with heart failure (HF). However, only a few large‐scale studies have identified the clinical utility of RDW ...after adjusting for covariates affecting RDW.
Methods and results
From January 2010 to April 2021, we retrospectively enrolled patients diagnosed with HF from three referral hospitals with available RDW data (taken within 3 months of HF diagnosis) using an integrated clinical data system. Patients with an ejection fraction (EF) < 50% or HFA‐PEFF (Heart Failure Association Pre‐test assessment, Echocardiography and natriuretic peptide, Functional testing, Final aetiology) score ≥ 2 without severe valvular heart disease or coronary revascularization were enrolled. The primary endpoint was all‐cause mortality, and cardiovascular mortality was also collected. Multivariable Cox regression analysis and stabilized inverse probability of treatment weighting (IPTW) were used to identify any association between RDW and all‐cause death by balancing covariates or compounding factors. The global χ2 score was calculated and discrimination analysis was performed to evaluate the incremental value of RDW in predicting prognosis. Among the 6599 participants enrolled in this study, 1256 (19.0%) cases of all‐cause death occurred, and the median duration of follow‐up was 887 (interquartile range 351–1589) days. Elevated RDW at the initial diagnosis was associated with poor prognosis cumulative incidence: 819 (30.2%) vs. 437 (11.2%), relative risk 1.58, 95% confidence interval (CI) 1.51–1.67, log‐rank P < 0.001. Multivariable Cox analysis showed that elevated RDW was a poor prognostic factor for the primary endpoint hazard ratio (HR) 1.11, 95% CI 1.06–1.16, P < 0.001, independent of clinical risk factors, N‐terminal pro‐brain natriuretic peptide (NT‐proBNP), and EF, which was concordant with the stabilized IPTW (HR 1.29, 95% CI 1.10–1.49, P < 0.001). Adding RDW to model composed of traditional risk factors, NT‐proBNP, and echocardiographic parameters showed incremental prognostic value for predicting poor prognosis (area under the receiver operating characteristic curve, 0.799–0.826; P < 0.001).
Conclusions
Increased RDW at the time of diagnosis is associated with poor prognosis in patients with HF, independent of clinical risk factors, such as NT‐proBNP, and echocardiographic parameters. Therefore, RDW may aid in the management of these patients beyond traditional risk factors.
Despite similar brachial blood pressure, central hemodynamics could be different. The objective of the present study was to investigate the factors, which could influence the discrepancy between ...central BP (cBP) and brachial blood pressure. Six hundred forty-seven patients (364 males, 48 ± 12 years old) were enrolled. Using applanation tonometry, cBP was noninvasively derived. The median difference between brachial systolic BP (bSBP) and central systolic BP (cSBP) was 8 mm Hg. We defined the discrepancy between bSBP and cSBP as differences >8 mm Hg. For adjustment of cBP, population was divided into 3 groups according to the cBP: group 1, <140 mm Hg of cSBP; group 2, 140 > cSBP < 160 mm Hg; group 3, =160 mm Hg of cSBP. All the central hemodynamic parameters of the patients, including augmentation pressure, augmentation index (AI), heart rate (75 bpm) adjusted augmentation index (AI@HR75), and subendocardial viability ratio, were measured. Using multivariate logistic regression analysis, we evaluated the factors which could influence the discrepancy between bSBP and cSBP. Age, gender, augmentation pressure, AI, and AI@HR75 were correlated with the discrepancy between bSBP and cSBP. AI@HR75 was significantly correlated with the discrepancy between bSBP and cSBP (β-coefficient = -0.376, P < .001 in group 1; β-coefficient = -0.297, P < .001 in group 2; and β-coefficient = -0.545, P < .001 in group 3). In groups 1 and 2, male gender was significantly correlated with the discrepancy between bSBP and cSBP (β-coefficient = -0.857, P = .035 in group 1; β-coefficient = -1.422, P = .039 in group 2). In present study, arterial stiffness might affect the discrepancy between bSBP and cSBP. Also, male gender was closely related to the discrepancy between bSBP and cSBP especially with cSBP <160 mm Hg. Not only cSBP, the discrepancy between cSBP and bSBP should be considered for understanding the central hemodynamics.
Atrial fibrillation (AF) has a heterogeneous pathophysiology according to individual patient characteristics. This study aimed to identify the effects of widely known risk factors on AF incidence ...according to age and to elucidate the clinical implications of these effects.
We analyzed data from 501,668 subjects (≥18years old) without AF and valvular heart disease from the Korean National Health Insurance Service-National Sample Cohort. The total population was divided into two groups according to age, <60years and ≥60years. AF occurred in 0.7% of the overall population (3,416 of 501,668) during the follow-up period (mean 47.6 months). In Cox regression analysis, age, male sex, previous ischemic stroke, heart failure, and hypertension were related to increased risk of new-onset AF in both age groups. Especially in the <60years age group, risk of new-onset AF was increased by relatively modifiable risk factors: obesity (body mass index ≥25kg/m2; hazard ratioHR 1.37 1.22-1.55, p<0.001, interaction p<0.001), and hypertension (HR 1.931.69-2.22, p<0.001, interaction p<0.001). Although interactions were not significant, chronic obstructive pulmonary disease (HR 1.411.24-1.60, p<0.001) and chronic kidney disease (HR 1.281.15-1.41, p<0.001) showed increased trends of the risk of new-onset AF in the ≥60years age group.
The risk profile for new-onset AF was somewhat different between the <60years and the ≥60years age groups. Compared to the ≥60years group, relatively modifiable risk factors (such as obesity and hypertension) had a greater impact on AF incidence in the <60years age group. Different management strategies to prevent AF development according to age may be needed.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Background
Although nonsustained ventricular tachycardia (NSVT) is a risk factor for sudden cardiac death in hypertrophic‐cardiomyopathy (HCM), the impact of premature ventricular contraction (PVC) ...burden, in the absence of NSVT, is not well‐known.
Hypothesis
PVC burden may be associated with myocardial fibrosis and genetic mutations in patients with HCM.
Methods
Of the 212 patients prospectively enrolled to the HCM registry of genetics, 84 were evaluated with both cardiac magnetic resonance, 24‐hour Holter monitoring and genetic analysis. Among them, 71 patients have not been diagnosed with NSVT.
Results
Patients with NSVT (n = 13) had a higher late gadolinium enhancement (LGE) amount, extracellular volume fraction (ECV), and prevalence of sarcomere mutations compared with patients without NSVT. Among patients without NSVT, those with LGE (n = 46) had a higher total PVC (109 ± 332 vs 7 ± 13, P = .003) and PVC burden (0.114 ± 0.225 vs 0.008 ± 0.014%, P = .003) during 24‐hour Holter monitoring compared with others. The %LGE and global ECV were correlated with PVC burden (r = 0.377, P = .001; r = 0.401, P = .001). The optimal cutoff value for PVC number for LGE was 45 (37.0% and 100% sensitivity and specificity, respectively) with 0.733 of the area under the receiver operating characteristic‐curve (P < .001). Thick filament gene mutation was more prevalent in the higher PVC burden group (41.2% vs 16.7%, P = .048).
Conclusion
Total PVC burden is significantly related to increase in myocardial fibrosis in HCM patients without NSVT.
To investigate the differential contribution of the left atrial (LA) function and left ventricular (LV) fibrosis to pulmonary arterial systolic pressure (PASP) in hypertrophic cardiomyopathy (HCM), ...dilated cardiomyopathy (DCM) and reperfused acute myocardial infarction (AMI).
Data of 370 patients with HCM (n = 133), DCM (n = 114) and reperfused AMI (n = 123) who underwent both echocardiography and cardiovascular magnetic resonance (CMR) were comprehensively reviewed. Phasic LA volumes, LA-global longitudinal strain (GLS), LA stiffness index, defined as E/e'/LA-GLS and extracellular volume fraction (ECV) of LV were measured using CMR.
E/e' was correlated with PASP in all groups; however, the predicted value was significantly attenuated after adjusting for LA volume and LA strain in HCM and DCM, but remained significant in AMI. The LA stiffness index was related to PASP in HCM (p = 0.01) and DCM (p = 0.03) independent of LA volume index and E/e', but not in AMI. In DCM, ECV was significantly related to PASP (p < 0.001) independent of LA volume index and E/e'. When subdivided according to the linear regression between PASP and E/e', patients in the discrepantly high PASP group had lower total emptying fraction and reservoir fraction of left atrium in HCM and DCM but not in AMI.
The LA function in HCM and DCM and LV fibrosis in DCM correlated with PASP independent of E/e' and LA size, contrary to that in AMI. These results suggest the presence of LA dysfunction in non-ischemic cardiomyopathies and usefulness of ECV measurement in DCM for the comprehensive evaluation of LV diastolic function.
Variability of blood pressure (BP) is known as a prognostic value for the subsequent target organ damage in hypertensive patients. Arterial stiffness is a risk factor for cardiovascular morbidity and ...mortality. The relationship between the arterial stiffness and the BP variability has been controversial. The objective of the present study was to investigate the relationship between arterial stiffness and home BP variability in patients with high normal BP and new onset hypertension (HTN).Four hundred sixty three patients (252 males, 49 ± 12 year-old) with high normal BP or HTN were enrolled. Using radial applanation tonometry, pulse wave analysis (PWA) was performed for evaluation of systemic arterial stiffness. All patients underwent both home BP monitoring (HBPM) and PWA. Home BP variability was calculated as the standard deviation (SD) of 7 measurements of HBPM. Multiple linear regression analysis was performed to estimate and test the independent effects of home BP variability on the arterial stiffness.Mutivariate analysis showed that both systolic and diastolic morning BP variabilities were correlated with arterial stiffness expressed as augmentation pressure (AP, β-coefficient = 1.622, P = .01 and β-coefficient = 1.07, P = .035). The SDs of systolic and diastolic BP of evening were also associated with AP (β-coefficient = 1.843, P = .001 and β-coefficient = 1.088, P = .036). The SDs of morning and evening systolic BP were associated with augmentation index (AI, β-coefficient = 1.583, P = .02 and β-coefficient = 1.792, P = .001) and heart rate (75 bpm) adjusted AI (β-coefficient = 1.592, P = .001 and β-coefficient = 1.792, P = .001).In present study, the variability of systolic BP was closely related with arterial stiffness. The home BP variability might be important indicator of arterial stiffness.
We evaluated the hemodynamic and geometric determinants of latent obstruction (LO, trans-left ventricular outflow tract (LVOT) gradient ≥30 mmHg with provocation) in patients with non-obstructive ...hypertrophic cardiomyopathy (HCMP). A total of 35 patients with non-obstructive HCMP underwent stepwise supine bicycle exercise echocardiography. Trans-LVOT pressure gradients, mitral geometric parameters, left ventricular ejection fractions (LVEF) and left ventricular end-systolic and diastolic dimensions (LVESD, LVEDD) were measured at each stage. The highest peak LVOT pressure gradient predominantly occurred immediately after exercise (n = 32, 91.3%) rather than during peak exercise (n = 3, 8.7%). Significant LO developed in nine patients (25%). No significant differences were found in resting echocardiographic parameters. Compared to the remaining patients, however, patients with LO had longer residual mitral leaflets (defined as residual portions of leaflets after coaptation; 4 ± 4 vs. 13 ± 4 mm, respectively; p = 0.001) and higher resting LVOT pressure gradients (7.4 ± 3.7 vs. 12.9 ± 5.8 mmHg, respectively; p = 0.001). Substantial decreases in mitral annular diameters from peak exercise to recovery after exercise were observed in the LO group, while mitral annular diameters increased after exercise in the non-LO group. In conclusion, the highest peak LVOT pressure gradient predominantly occurred immediately after exercise rather than during peak exercise, regardless of LO. Abrupt decrease of mitral annular diameter immediately after exercise, a longer residual mitral leaflet and a higher resting LVOT pressure gradient at rest might be related to LO.
Myocardial fibrosis is an important prognostic factor in hypertrophic cardiomyopathy (HCM). However, the contribution from a wide spectrum of genetic mutations has not been well defined. We sought to ...investigate effect of sarcomere and mitochondria-related mutations on myocardial fibrosis in HCM.
In 133 HCM patients, comprehensive genetic analysis was performed in 82 nuclear DNA (33 sarcomere-associated genes, 5 phenocopy genes, and 44 nuclear genes linked to mitochondrial cardiomyopathy) and 37 mitochondrial DNA. In all patients, cardiovascular magnetic resonance (CMR) was performed, including 16-segmental thickness, late gadolinium enhancement (LGE), native and post-T1, extracellular volume fraction (ECV), and T2, along with echo-Doppler evaluations.
Patients with sarcomere mutation (SM, n = 41) had higher LGE involved segment, % LGE mass, ECV and lower post-T1 compared to patients without SM (n = 92, all p < 0.05). When classified into, non-mutation (n = 67), only mitochondria-related mutation (MM, n = 24), only-SM (n = 36) and both SM and MM (n = 5) groups, only-SM group had higher ECV and LGE than the non-mutation group (all p < 0.05). In non-LGE-involved segments, ECV was significantly higher in patients with SM. Within non-SM group, patients with any sarcomere variants of uncertain significance had higher echocardiographic Doppler E/e' (p < 0.05) and tendency of higher LGE amount and ECV (p > 0.05). However, MM group did not have significantly higher ECV or LGE amount than non-mutation group.
SMs are significantly related to increase in myocardial fibrosis. Although, some HCM patients had pathogenic MMs, it was not associated with an increase in myocardial fibrosis.
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