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Pubblicazioni recenti - cardiovascular disease
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Personalized Prediction of Cardiovascular Benefits and Bleeding Harms From Aspirin for Primary Prevention: A Benefit-Harm Analysis.
Ann Intern Med2019 Sep;():. doi: 10.7326/M19-1132.
Selak Vanessa, Jackson Rod, Poppe Katrina, Wu Billy, Harwood Matire, Grey Corina, Pylypchuk Romana, Mehta Suneela, Choi Yeun-Hyang, Kerr Andrew, Wells Sue,
Abstract
Background:
Whether the benefits of aspirin for the primary prevention of cardiovascular disease (CVD) outweigh its bleeding harms in some patients is unclear.
Objective:
To identify persons without CVD for whom aspirin would probably result in a net benefit.
Design:
Individualized benefit-harm analysis based on sex-specific risk scores and estimates of the proportional effect of aspirin on CVD and major bleeding from a 2019 meta-analysis.
Setting:
New Zealand primary care.
Participants:
245 028 persons (43.6% women) aged 30 to 79 years without established CVD who had their CVD risk assessed between 2012 and 2016.
Measurements:
The net effect of aspirin was calculated for each participant by subtracting the number of CVD events likely to be prevented (CVD risk score × proportional effect of aspirin on CVD risk) from the number of major bleeds likely to be caused (major bleed risk score × proportional effect of aspirin on major bleeding risk) over 5 years.
Results:
2.5% of women and 12.1% of men were likely to have a net benefit from aspirin treatment for 5 years if 1 CVD event was assumed to be equivalent in severity to 1 major bleed, increasing to 21.4% of women and 40.7% of men if 1 CVD event was assumed to be equivalent to 2 major bleeds. Net benefit subgroups had higher baseline CVD risk, higher levels of most established CVD risk factors, and lower levels of bleeding-specific risk factors than net harm subgroups.
Limitations:
Risk scores and effect estimates were uncertain. Effects of aspirin on cancer outcomes were not considered. Applicability to non-New Zealand populations was not assessed.
Conclusion:
For some persons without CVD, aspirin is likely to result in net benefit.
Primary Funding Source:
Health Research Council of New Zealand.
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Subclinical cardiac stiffness is associated with arterial stiffness in healthy young nulligravid women: Potential links to preeclampsia.
Pregnancy Hypertens2019 Sep;18():49-54. doi: S2210-7789(19)30349-6.
Cooper Kylie M, Barrett Trace, McBride Carole A, Badger Gary J, Steiner Johannes, LeWinter Martin M, Bernstein Ira M,
Abstract
OBJECTIVES:
Preeclampsia is an independent risk factor for subsequent cardiovascular disease and diastolic dysfunction and has been linked to arterial stiffness. We hypothesized that arterial stiffness would be associated with echocardiographic markers of diastolic dysfunction in healthy nulligravid women.
STUDY DESIGN:
31 healthy nulligravid women underwent assessment of peripheral arterial stiffness via aorto-femoral pulse wave velocity, popliteal distensibility and ? stiffness measures as well as hemodynamic response to volume challenge. 22 underwent cardiac assessment via conventional and stress echocardiography with a focus on diastolic function utilizing tissue/pulse wave Doppler imaging and 3D speckle tracking. Bivariate associations between variables were evaluated using correlation coefficients (Pearson r) and Student's t-tests.
RESULTS:
No participants had echocardiographic values meeting criteria for overt diastolic dysfunction. Baseline global circumferential strain was significantly correlated with distensibility and ? stiffness (n?=?18, r?=?-0.61, p?=?0.007, n?=?18, r?=?0.56, p?=?0.01). Peak deceleration time was correlated with ?stiffness (n?=?9; r?=?0.80, p?=?0.01). Pulse wave velocity was not significantly correlated with cardiac measures (p?>?0.05). Family history of a first or second degree relative with myocardial infarction or hypertension was associated with decreased popliteal artery distensibility (p?=?0.02 and p?=?0.03, respectively).
CONCLUSIONS:
In healthy nulligravid women there is evidence that markers of decreased left ventricular relaxation are associated with increased peripheral vascular stiffness as is a family history of myocardial infarction or hypertension. These findings raise the possibility that the diastolic dysfunction and arterial stiffness observed in the setting of preeclampsia are driven by underlying properties present prior to pregnancy and contribute to lifetime cardiovascular risk.
Copyright © 2019 International Society for the Study of Hypertension in Pregnancy. Published by Elsevier B.V. All rights reserved.
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Resilience among older cardiovascular disease patients with probable sarcopenia.
Arch Gerontol Geriatr2019 Aug;86():103939. doi: S0167-4943(19)30182-7.
Lee Szu-Ying, Tung Heng-Hsin, Peng Li-Ning, Chen Liang-Kung, Hsu Ching-I, Huang Yen-Ling,
Abstract
AIM AND OBJECTIVES:
The purpose of this study was to investigate the factors associated with resilience among probable sarcopenia older adults with cardiovascular disease.
INTRODUCTION:
Resilience has been reported to be positively correlated with the mental health and physical functioning of older adults. Previous research has found that the development of resilience constitutes a form of compensation for loss of physical health. It is important for older adults, especially those with other underlying conditions, such as cardiovascular disease and sarcopenia, to have the ability to overcome adversity during the aging process. Thus, resilience becomes a critical characteristic in achieving a better life.
METHODS:
A cross-sectional study design was used. A demographic questionnaire and the Chinese version of the Resilience Scale (CRS) were used to collect data. Multiple logistic regression was used to evaluate the predictors of low resilience.
RESULTS:
A total of 267 participants were recruited, including 126 females and 141 males. Of the participants, 56% of their scores indicated low resilience. Income, education level, exercise time, primary caregiver, and having hypertension were the predictors of resilience.
CONCLUSION:
The population with sarcopenia is increasing worldwide. Understanding resilience levels among older adults with probable sarcopenia is essential for promoting their mental health. Clinicians can use the results of this study to identify populations at high risk for low resilience and design specific interventions to promote better health outcomes.
Copyright © 2019 Elsevier B.V. All rights reserved.
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The impact of physiological stress conditions on protein structure and trypsin inhibition of serine protease inhibitor Kazal type 1 (SPINK1) and its N34S variant.
Biochim Biophys Acta Proteins Proteom2019 Sep;():140281. doi: S1570-9639(19)30167-0.
Buchholz Ina, Nagel Felix, Klein Annelie, Wagh Preshit R, Mahajan Ujjwal M, Greinacher Andreas, Lerch Markus M, Mayerle Julia, Delcea Mihaela,
Abstract
One of the most common mutations in the serine protease inhibitor Kazal type 1 (SPINK1) gene is the N34S variant which is strongly associated with chronic pancreatitis. Although it is assumed that N34S mutation constitutes a high-risk factor, the underlying pathologic mechanism is still unknown. In the present study, we investigated the impact of physiological stress factors on SPINK1 protein structure and trypsin inhibitor function using biophysical methods. Our circular dichroism spectroscopy data revealed differences in the secondary structure of SPINK1 and N34S mutant suggesting protein structural changes induced by the mutation as an impairment that could be disease-relevant. We further confirmed that both SPINK1 (K of 0.15?±?0.06?nM) and its N34S variant (K of 0.08?±?0.02?nM) have similar binding affinity and inhibitory effect towards trypsin as shown by surface plasmon resonance and trypsin inhibition assay studies, respectively. We found that stress conditions such as altered ion concentrations (i.e. potassium, calcium), temperature shifts, as well as environmental pH lead to insignificant differences in trypsin inhibition between SPINK1 and N34S mutant. However, we have shown that the environmental pH induces structural changes in both SPINK1 constructs in a different manner. Our findings suggest protein structural changes in the N34S variant as an impairment of SPINK1 and environmental pH shift as a trigger that could play a role in disease progression of pancreatitis.
Copyright © 2019. Published by Elsevier B.V.
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Ciprofibrate attenuates airway remodeling in cigarette smoke-exposed rats.
Respir Physiol Neurobiol2019 Sep;():103290. doi: S1569-9048(19)30160-0.
Ke Qian, Yang Lin, Cui Qinghua, Diao Wenqi, Zhang Youyi, Xu Ming, He Bei,
Abstract
Airway remodeling is a key pathological lesion in chronic obstructive pulmonary disease (COPD), and it leads to poorly reversible airway obstruction. Current pharmacological interventions are ineffective at controlling airway remodeling. To address this issue, we queried the Connectivity Map (cMap) database to screen for drug candidates that had the potential to dilate the bronchus and inhibit airway smooth muscle (ASM) proliferation. We identified ciprofibrate as a drug candidate. Ciprofibrate inhibited cigarette smoke extract-induced rat ASM cell contraction and proliferation in vitro. We exposed Sprague-Dawley (SD) rats to clean air or cigarette smoke (CS) and treated the rats with ciprofibrate. Ciprofibrate improved pulmonary function, inhibited airway hypercontraction, and ameliorated morphological small airway remodeling, including airway smooth muscle proliferation, in CS-exposed rats. Ciprofibrate also significantly reduced IL-1?, IL-12p70, IL-17A and IL-18 expression, which are related to airway remodeling, in the sera of CS-exposed rats. These findings indicate that ciprofibrate could attenuate airway remodeling in CS-exposed rats.
Copyright © 2019. Published by Elsevier B.V.
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A new approach to the diagnosis and treatment of atherosclerosis: the era of the liposome.
Drug Discov Today2019 Sep;():. doi: S1359-6446(19)30349-6.
Kiaie Nasim, Gorabi Armita Mahdavi, Penson Peter E, Watts Gerald, Johnston Thomas P, Banach Maciej, Sahebkar Amirhossein,
Abstract
The consequences of atherosclerotic cardiovascular disease (ASCVD) include myocardial infarction, ischemic stroke, and angina pectoris, which are major causes of mortality and morbidity worldwide. Despite current therapeutic strategies to reduce risk, patients still experience the consequences of ASCVD. Consequently, a current goal is to enhance visualization of early atherosclerotic lesions to improve residual ASCVD risk. The uses of liposomes, in the context of ASCVD, can include as contrast agents for imaging techniques, as well as for the delivery of antiatherosclerotic drugs, genes, and cells to established sites of plaque. Additionally, liposomes have a role as vaccine adjuvants against mediators of atherosclerosis. Here. we review the scientific and clinical evidence relating to the use of liposomes in the diagnosis and management of ASCVD.
Copyright © 2019 Elsevier Ltd. All rights reserved.
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Recent progress in the small-molecule fluorescent probes for the detection of sulfur dioxide derivatives (HSO/SO).
Free Radic Biol Med2019 Sep;():. doi: S0891-5849(19)30666-5.
Yang Bing, Xu Jing, Zhu Hai-Liang,
Abstract
Sulfur dioxide (SO) had been recognized as an environmental pollutant produced from industrial processes. SO is water soluble and forms hydrated SO (SO·HO), bisulfite ion (HSO), and sulfite ion (SO) upon dissolution in water. SO could be also produced endogenously from sulfur-containing amino acids l-cysteine in mammals. Endogenous SO can maintain the balance of biological sulfur and redox equilibrium in vivo, regulate blood insulin levels and reduce blood pressure. Excess intake of exogenous SO can result in respiratory diseases, cardiovascular diseases and neurological disorders. As a result, fluorescent probes to detect HSO/SO have attracted great attention in recent years. Herein, a general overview was provided with the aim to highlight the typical examples of the HSO/SO fluorescent probes reported since 2010, especially those in the past five years. We have classified HSO/SO fluorescent probes through different chemical reaction mechanisms and wish this review will give some help to the researchers in this field.
Copyright © 2019. Published by Elsevier Inc.
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Redox signaling in ischemic postconditioning protection involves PKC? and Erk1/2 pathways and converges indirectly in Nrf2 activation.
Cell Signal2019 Sep;():109417. doi: S0898-6568(19)30213-X.
Díaz-Ruíz Jorge-Luis, Macías-López Arturo, Alcalá-Vargas Francisco, Guevara-Chávez José-Guadalupe, Mejía-Uribe Aída, Silva-Palacios Alejandro, Zúñiga-Muñoz Alejandra, Zazueta Cecilia, Buelna-Chontal Mabel,
Abstract
Ischemic-postconditioning (iPostC) exerts cardioprotection by preserving redox homeostasis in the reperfused heart. This protective effect has been associated with the activation of endogenous antioxidant response driven by transcription factor Nrf2 and with the activation of 'reperfusion injury salvage kinases' (RISK) as PI3K, PKC and Erk1/2. Redox homeostasis is essential for normal cell physiology since reactive oxygen species (ROS) are crucial for processes that involve protein signaling. Thus, it has become clear that not only the perturbation of redox balance to oxidative state is deleterious but also towards a reductive state contributing to pathogenesis of diseases. However, there is still a scarce knowledge about the role of ROS in the cardioprotective signals mediated by RISK in postconditioned hearts. Therefore, we studied the role of ROS as initiator of RISK signaling molecules in iPostC-conferred cardioprotection. With the aim to study the relationship between redox-dependent RISK activation and the downstream activation of the transcription factor Nrf2, we evaluated the effect of redox signaling disruption by the effect of ascorbic acid in iPostC hearts. Our results showed that PKC? and Erk1/2 activation is redox-dependent and that concurs downstream with Nrf2 deficient activation. Besides, using inhibitors we found that neither PI3K nor Erk1/2 are directly related with Nrf2 activation, indicating that these kinases have other targets. We conclude that redox signaling participates in cardioprotection triggered by iPostC through the action of kinase-dependent and -independent mechanisms and concurred with the downstream regulation of Nrf2-mediated antioxidant response to prolonged redox balance during long reperfusion.
Copyright © 2018. Published by Elsevier Inc.
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Hemodynamic Phenotypes of Hypertension Based on Cardiac Output and Systemic Vascular Resistance.
Am J Med2019 Sep;():. doi: S0002-9343(19)30766-1.
Mahajan Shiwani, Gu Jianlei, Lu Yuan, Khera Rohan, Spatz Erica S, Zhang MaoZhen, Sun NingLing, Zheng Xin, Zhao Hongyu, Lu Hui, Ma Zheng J, Krumholz Harlan M,
Abstract
BACKGROUND:
Blood pressure is a physiologic measure that reflects cardiac output and systemic vascular resistance. Classification by these components could be useful in characterizing subtypes of hypertension which may have a role in selecting treatment strategies. However, hemodynamic phenotypes of a large, stable, outpatient population with hypertension remain unknown.
METHODS:
We included 34,238 people, with systolic blood pressure of ?130mmHg, who underwent impedance cardiography at 51 sites of iKang Health Checkup Centers throughout China between 2012 and 2018. Hemodynamic parameters measured included: stroke volume, stroke volume index, heart rate, cardiac output, cardiac index, systemic vascular resistance, and systemic vascular resistance index. We characterized these by systolic blood pressure categories and assessed patient characteristics associated with the ratio of cardiac index to systemic vascular resistance index.
RESULTS:
Among the study cohort (n=33,414; mean age 52±13years; 36.6% female), 49%, 40%, and 11% had systolic blood pressure130-139, 140-159, and?160mmHg, respectively. Among patients with systolic blood pressure 140-159mmHg, 9353 (70%) had high systemic vascular resistance index but normal/low cardiac index, 1949 (15%) had high cardiac index but low/normal systemic vascular resistance index, and 2053 (15%) had low/normal cardiac index and systemic vascular resistance index. Using multivariable analysis, we found that cardiac index to systemic vascular resistance index ratio was negatively associated with age and body mass index (all P<0.05; R-square 0.16, 0.12 and 0.09 for systolic blood pressure 130-139, 140-159 and?160mmHg, respectively).
CONCLUSIONS:
Different hemodynamic blood pressure phenotypes were identified across all hypertensive blood pressure categories. While individual characteristics were associated with the cardiac index to systemic vascular resistance index ratio, they only weakly explained the variation.
Copyright © 2019. Published by Elsevier Inc.
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The homozygous variant c.245G>A/p.G82D in PNPLA2 is associated with arrhythmogenic cardiomyopathy phenotypic manifestations.
Clin Genet2019 Sep;():. doi: 10.1111/cge.13642.
Rao Man, Guo Guang-Ran, Li Meng-Meng, Chen Shi, Chen Kai, Chen Xiao, Song Jiang-Ping, Hu Sheng-Shou,
Abstract
Arrhythmogenic cardiomyopathy (ACM) is a familial cardiomyopathy featured by fibro-fatty replacement of cardiomyocytes. Responsible genetic factors are not discernible in approximately one third of ACM probands. To investigate this further, we performed whole genome sequencing (WGS) in 14 mutation-negative ACM probands who underwent cardiac transplantation, and we identified one ACM proband with a rare homozygous missense variant in PNPLA2 (c.245G>A, p.G82D), a rate-limiting enzyme that hydrolyzes triglycerides into fatty-acids and diacylglycerol. Bioinformatic analysis suggested that this missense variant may lead to loss-of-function and therefore impair lipid catabolism. Genetic screening in this proband's family also inferred that the homozygous variant co-segregated with disease. To validate the pathogenicity of this variant and confirm its association with ACM, we established a knock-in mouse model carrying the orthologous human homozygous PNPLA2 variant. Interestingly, mice with the homozygous variant presented with arrhythmias and significant cardiac dysfunction at 12-weeks, whereas heterozygous mice were not affected. Moreover, those homozygous mice suffered sudden death and/or heart failure by age of 14-weeks. Pathological examination showed that extensive lipogenesis in cardiomyocytes and cardiac fibrosis were prominent in the myocardium. Herein, our data demonstrated that the homozygous missense variant PNPLA2 (c.245G>A, p.G82D) associated with a recessive form of ACM. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
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Myocardial Adaptations to Competitive Swim Training.
Med Sci Sports Exerc2019 Oct;51(10):1987-1994. doi: 10.1249/MSS.0000000000002022.
Wasfy Meagan M, Weiner Rory B, Wang Francis, Berkstresser Brant, Deluca James, Hutter Adolph M, Picard Michael H, Baggish Aaron L,
Abstract
PURPOSE:
Swim training is performed in the prone or supine position and obligates water immersion, factors that may augment cardiac volume loading more than other endurance sports. At present, prospective data defining the cardiac responses to swim training are lacking. We therefore studied myocardial adaptations among competitive swimmers to establish a causal relationship between swim training and left ventricular (LV) remodeling.
METHODS:
Collegiate swimmers were studied before and after a 90-d period of training intensification. Transthoracic echocardiography was used to examine LV structural and functional adaptations under resting conditions and during an acute LV afterload challenge generated by isometric handgrip testing (IHGT). A sedentary control population was identically studied with IHGT.
RESULTS:
In response to a discrete period of swim training intensification, athletes (n = 17, 47% female, 19 ± 0.4 yr old) experienced eccentric LV remodeling, characterized by proportionally more chamber dilation than wall thickening, with attendant enhancements of resting LV systolic (LV twist) and diastolic (early and late phase tissue velocities) function. Compared with baseline and controls, athletes posttraining demonstrated greater systolic twist impairment during IHGT. However, training-induced LV dilation coupled with gains in diastolic function offsets this acquired systolic susceptibility to acute afterload, resulting in the relative preservation of stroke volume during IHGT.
CONCLUSION:
Swim training, a sport characterized by unique cardiac loading conditions, stimulates eccentric LV remodeling with the concomitant augmentation of systolic twist and diastolic relaxation. This volume-mediated cardiac remodeling appears to result in greater systolic susceptibility to acute afterload challenge. Further work is required to establish how training-induced changes in function translate to human performance and whether these are accompanied by physiologic trade-offs with relevance to common forms of heart disease.
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Measuring lower limb circumference and volume - introduction of a novel optical 3D volumetric measurement system.
Biomed Tech (Berl)2019 Sep;():. doi: 10.1515/bmt-2018-0100.
Tischer Thomas, Oye Sebastian, Wolf Andreas, Feldhege Frank, Jacksteit Robert, Mittelmeier Wolfram, Bader Rainer, Mau-Moeller Anett,
Abstract
This study comprised two experiments: (1) the reliability of a novel optical three-dimensional (3D) volumetric measurement system (BODYTRONIC® 600) for the assessment of lower limb circumference and volume; (2) the comparison of data obtained from BODYTRONIC® 600 with that provided by computed tomography (CT) for accuracy estimation. Reliability was assessed in 20 healthy subjects. Accuracy was determined by comparing the deviations in the surface topology of two 3D models obtained from BODYTRONIC® 600 and CT. Reliability was very high for leg circumference measures [coefficient of variations (CVs) range 0.3%-1.3%] and slightly lower for foot circumference (CVs around 2.0%). Reliability of leg volume was also found to be very high (CVs???2.5%). Differences in surface topology between BODYTRONIC® 600 and CT were primarily below 1 mm indicating high accuracy. The volumes of the foot were higher (range 0.9%-1.7%) and that of the leg, lower (range 1.0%-1.3%) compared to CT. The BODYTRONIC® 600 system provides fast, highly reliable and accurate measures of lower limb circumference and volume and can be considered as a valuable measurement tool for use in various research and clinical applications.
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Do We Need an Apgar Score for Older Adults?
Circulation2019 Sep;140(12):973-975. doi: 10.1161/CIRCULATIONAHA.119.039670.
Wenger Nanette K,
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Prognostic Value of Coronary Microvascular Function Measured Immediately After Percutaneous Coronary Intervention in Stable Coronary Artery Disease: An International Multicenter Study.
Circ Cardiovasc Interv2019 Sep;12(9):e007889. doi: 10.1161/CIRCINTERVENTIONS.119.007889.
Nishi Takeshi, Murai Tadashi, Ciccarelli Giovanni, Shah Sonia V, Kobayashi Yuhei, Derimay François, Waseda Katsuhisa, Moonen Avalon, Hoshino Masahiro, Hirohata Atsushi, Yong Andy S C, Ng Martin K C, Amano Tetsuya, Barbato Emanuele, Kakuta Tsunekazu, Fearon William F,
Abstract
BACKGROUND:
The prognostic impact of coronary microvascular dysfunction after percutaneous coronary intervention (PCI) remains unclear in patients with stable coronary artery disease. This study sought to investigate the prognostic value of microvascular function measured immediately after PCI in patients with stable coronary artery disease.
METHODS:
We enrolled 572 patients with stable coronary artery disease who underwent PCI and elective measurement of the index of microcirculatory resistance (IMR) immediately after PCI from 8 centers in 4 countries. Impaired microvascular function was defined as IMR?25 (high IMR). Major adverse cardiac events, including death, myocardial infarction (MI) and target vessel revascularization, were evaluated.
RESULTS:
During a median follow-up duration of 4.0 years, the cumulative major adverse cardiac events rate was significantly higher in the high IMR group (n=66/148) compared with the low IMR group (n=128/424; hazard ratio [HR], 1.56; 95% CI, 1.16-2.105; =0.001), primarily due to a higher rate of periprocedural MI (HR, 1.59; 95% CI, 1.11-2.28; =0.004) but also due to higher rates of mortality (HR, 1.59; 95% CI, 0.76-3.35; =0.22), spontaneous MI (HR, 2.10; 95% CI, 0.67-6.63; =0.20) and target vessel revascularization (HR, 1.40; 95% CI, 0.77-2.54; =0.27). Cumulative risk for death, spontaneous MI, and target vessel revascularization was higher in the high IMR group (HR, 1.55; 95% CI, 0.99-2.43; =0.056), as was death and spontaneous MI alone (HR, 1.79; 95% CI, 0.96-3.36; =0.065). On multivariable analysis, high IMR post-PCI was an independent predictor of major adverse cardiac events.
CONCLUSIONS:
IMR measured immediately after PCI predicts adverse events in patients with stable coronary artery disease.
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Optimal Cutoff Value of Fractional Flow Reserve Derived From Coronary Computed Tomography Angiography for Predicting Hemodynamically Significant Coronary Artery Disease.
Circ Cardiovasc Imaging2019 Aug;12(8):e008905. doi: 10.1161/CIRCIMAGING.119.008905.
Matsumura-Nakano Yukiko, Kawaji Tetsuma, Shiomi Hiroki, Kawai-Miyake Kanae, Kataoka Masako, Koizumi Koji, Matsuda Akira, Kitano Kazuki, Yoshida Masaharu, Watanabe Hirotoshi, Tazaki Junichi, Kato Takao, Saito Naritatsu, Shizuta Satoshi, Ono Koh, Togashi Kaori, Morimoto Takeshi, Kimura Takeshi,
Abstract
BACKGROUND:
The optimal cutoff value of fractional flow reserve (FFR) derived from coronary computed tomography angiography (FFR) remains unclear.
METHODS:
The current study population consisted of 93 patients with 139 vessels, who had suspected coronary artery disease by computed tomography angiography and underwent invasive FFR. We evaluated diagnostic performance of FFR according to different FFR cutoff values and FFR ranges with invasive FFR ?0.80 as the reference standard.
RESULTS:
In per-vessel analysis, median invasive FFR was 0.85 (interquartile range, 0.75-0.90), and 57 out of 139 vessels (41%) showed hemodynamically significant stenosis (?0.80). Median FFR was 0.77 (interquartile range, 0.66-0.84; mean difference [invasive FFR-FFR], 0.06±0.11). Per-vessel accuracy, sensitivity, specificity, positive predictive value, and negative predictive value were 73%, 95%, 59%, 61%, and 94% for the cutoff value of FFR ?0.80, 81%, 86%, 78%, 73%, and 89% for FFR ?0.75, and 83%, 74%, 89%, 82%, and 83% for FFR ?0.70, respectively. Per-vessel accuracy across the different ranges of FFR ?0.60, 0.61 to 0.70, 0.71 to 0.80, 0.81 to 0.90, and >0.90 with the cutoff value of FFR ?0.80 were 95%, 74%, 32%, 93%, and 100%, respectively. Setting a gray zone of FFR 0.71 to 0.80 provided high positive predictive value (82%; n=42/51) in the range of FFR ?0.70 and high negative predictive value (94%; n=48/51) in FFR >0.80.
CONCLUSIONS:
This study suggested that referral to invasive coronary angiography should be considered individually in the range of FFR 0.71 to 0.80, whereas dichotomous decision could be made in FFR ?0.70 and >0.80. Future prospective studies evaluating clinical outcomes are needed to establish optimal FFR-based diagnostic algorithm.
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Minding the Microcirculation: Is it Worth the Effort?
Circ Cardiovasc Interv2019 Sep;12(9):e008312. doi: 10.1161/CIRCINTERVENTIONS.119.008312.
Claessen Bimmer E, Cao Davide, Mehran Roxana,
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Automated and Interpretable Patient ECG Profiles for Disease Detection, Tracking, and Discovery.
Circ Cardiovasc Qual Outcomes2019 Sep;12(9):e005289. doi: 10.1161/CIRCOUTCOMES.118.005289.
Tison Geoffrey H, Zhang Jeffrey, Delling Francesca N, Deo Rahul C,
Abstract
BACKGROUND:
The ECG remains the most widely used diagnostic test for characterization of cardiac structure and electrical activity. We hypothesized that parallel advances in computing power, machine learning algorithms, and availability of large-scale data could substantially expand the clinical inferences derived from the ECG while at the same time preserving interpretability for medical decision-making.
METHODS AND RESULTS:
We identified 36?186 ECGs from the University of California, San Francisco database that would enable training of models for estimation of cardiac structure or function or detection of disease. We segmented the ECG into standard component waveforms and intervals using a novel combination of convolutional neural networks and hidden Markov models and evaluated this segmentation by comparing resulting electrical intervals against 141?864 measurements produced during the clinical workflow. We then built a patient-level ECG profile, a 725-element feature vector and used this profile to train and interpret machine learning models for examples of cardiac structure (left ventricular mass, left atrial volume, and mitral annulus e-prime) and disease (pulmonary arterial hypertension, hypertrophic cardiomyopathy, cardiac amyloid, and mitral valve prolapse). ECG measurements derived from the convolutional neural network-hidden Markov model segmentation agreed with clinical estimates, with median absolute deviations as a fraction of observed value of 0.6% for heart rate and 4% for QT interval. Models trained using patient-level ECG profiles enabled surprising quantitative estimates of left ventricular mass and mitral annulus e' velocity (median absolute deviation of 16% and 19%, respectively) with good discrimination for left ventricular hypertrophy and diastolic dysfunction as binary traits. Model performance using our approach for disease detection demonstrated areas under the receiver operating characteristic curve of 0.94 for pulmonary arterial hypertension, 0.91 for hypertrophic cardiomyopathy, 0.86 for cardiac amyloid, and 0.77 for mitral valve prolapse.
CONCLUSIONS:
Modern machine learning methods can extend the 12-lead ECG to quantitative applications well beyond its current uses while preserving the transparency that is so fundamental to clinical care.
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Saphenous Vein Graft Pseudoaneurysm Causing External Compression of the Pulmonary Artery.
Circ Cardiovasc Imaging2019 Aug;12(8):e009377. doi: 10.1161/CIRCIMAGING.119.009377.
Duran Crane Alejandro, Newtown Emily, Cremer Paul, Edward Montané Bryce, Xu Bo,
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Effect of Baseline Left Ventricular Ejection Fraction on 2-Year Outcomes After Transcatheter Aortic Valve Replacement: Analysis of the PARTNER 2 Trials.
Circ Heart Fail2019 Aug;12(8):e005809. doi: 10.1161/CIRCHEARTFAILURE.118.005809.
Furer Ariel, Chen Shmuel, Redfors Bjorn, Elmariah Sammy, Pibarot Philippe, Herrmann Howard C, Hahn Rebecca T, Kodali Susheel, Thourani Vinod H, Douglas Pamela S, Alu Maria C, Fearon William F, Passeri Jonathan, Malaisrie S Chris, Crowley Aaron, McAndrew Thomas, Genereux Philippe, Ben-Yehuda Ori, Leon Martin B, Burkhoff Daniel,
Abstract
BACKGROUND:
Impaired left ventricular function is associated with worse prognosis among patients with aortic stenosis treated medically or with surgical aortic valve replacement. It is unclear whether reduced left ventricular ejection fraction (LVEF) is an independent predictor of adverse outcomes after transcatheter aortic valve replacement.
METHODS AND RESULTS:
Patients who underwent transcatheter aortic valve replacement in the PARTNER 2 trials (Placement of Aortic Transcatheter Valves) and registries were stratified according to presence of reduced LVEF (<50%) at baseline, and 2-year risk of cardiovascular mortality was compared using Kaplan-Meier methods and multivariable Cox proportional hazards regression. Of 2991 patients, 839 (28%) had reduced LVEF. These patients were younger, more often males, and were more likely to have comorbidities, such as coronary disease, diabetes mellitus, and renal insufficiency. Compared with patients with normal LVEF, patients with low LVEF had higher crude rates of 2-year cardiovascular mortality (19.8% versus 12.0%, <0.0001) and all-cause mortality (27.4% versus 19.2%, <0.0001). Mean aortic valve gradient was not associated with clinical outcomes other than heart failure hospitalizations (hazard ratio [HR], 0.99; CI, 0.99-1.00; =0.03). After multivariable adjustment, patients with reduced versus normal LVEF had significantly higher adjusted risk of cardiovascular death (adjusted HR, 1.42, 95% CI, 1.11-1.81; =0.005), but not all-cause death (adjusted HR, 1.20; 95% CI, 0.99-1.47; =0.07). When LVEF was treated as continuous variable, it was associated with increased 2-year risk of both cardiovascular mortality (adjusted HR per 10% decrease in LVEF, 1.16; 95% CI, 1.07-1.27; =0.0006) and all-cause mortality (adjusted HR, 1.09; 95% CI, 1.01-1.16; =0.02).
CONCLUSIONS:
In this patient-level pooled analysis of PARTNER 2 patients who underwent transcatheter aortic valve replacement, baseline LVEF was an independent predictor of 2-year cardiovascular mortality.
CLINICAL TRIAL REGISTRATION:
URL: https://www.clinicaltrials.gov. Unique identifiers: NCT01314313, NCT02184442, NCT03222128, and NCT02184441.
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Association Between Low-Dose Rivaroxaban With or Without Aspirin and Ischemic Stroke Subtypes: A Secondary Analysis of the COMPASS Trial.
JAMA Neurol2019 Sep;():. doi: 10.1001/jamaneurol.2019.2984.
Perera Kanjana S, Ng Kelvin K H, Nayar Sumiti, Catanese Luciana, Dyal Leanne, Sharma Mukul, Connolly Stuart J, Yusuf Salim, Bosch Jackie, Eikelboom John W, Hart Robert G,
Abstract
Importance:
The COMPASS (Cardiovascular Outcomes for People Using Anticoagulation Strategies) randomized clinical trial was stopped early owing to the efficacy of low-dose rivaroxaban plus aspirin in preventing major cardiovascular events. The main reason for early trial termination was the effect of combination therapy on reducing ischemic strokes.
Objective:
To analyze the association between low-dose rivaroxaban with or without aspirin and different ischemic stroke subtypes.
Design, Setting, and Participants:
This is a secondary analysis of a multicenter, double-blind, randomized, placebo-controlled study that was performed in 33 countries from March 12, 2013, to May 10, 2016. Patients with stable atherosclerotic vascular disease were eligible, and a total of 27?395 participants were randomized and followed up to February 6, 2017. All first ischemic strokes and uncertain strokes that occurred by this date were adjudicated using TOAST (Trial of Org 10172 in Acute Stroke Treatment) criteria. The analysis of ischemic stroke subtypes was evaluated using an intention-to-treat principle. Statistical analysis was performed from March 12, 2013, to February 6, 2017.
Interventions:
Participants received rivaroxaban (2.5 mg twice a day) plus aspirin (100 mg once a day), rivaroxaban (5 mg twice a day), or aspirin (100 mg once a day).
Main Outcomes and Measures:
Risk of ischemic stroke subtypes during follow-up.
Results:
A total of 291 patients (66 women; mean [SD] age, 69.4 [8.5] years; 43 [14.8%] had a previous nonlacunar stroke) experienced an ischemic stroke. During the study, 49 patients (16.8%) received a diagnosis of atrial fibrillation. Applying TOAST criteria, 59 strokes (20.3%) were cardioembolic, 54 strokes (18.6%) were secondary to greater than 50% stenosis of the ipsilateral internal carotid artery, 42 strokes (14.4%) had a negative evaluation that met criteria for embolic stroke of undetermined source, and 21 strokes (7.2%) were secondary to small vessel disease. There were significantly fewer cardioembolic strokes (hazard ratio [HR], 0.40 [95% CI, 0.20-0.78]; P?=?.005) and embolic strokes of undetermined source (HR, 0.30 [95% CI, 0.12-0.74]; P?=?.006) in the combination therapy group compared with the aspirin-only group. A trend for reduction in strokes secondary to small vessel disease (HR, 0.36 [95% CI, 0.12-1.14]; P?=?.07) was not statistically significant. No significant difference was observed between the 2 groups in strokes secondary to greater than 50% carotid artery stenosis (HR, 0.85 [95% CI, 0.45-1.60]; P?=?.61). Rivaroxaban, 5 mg, twice daily showed a trend for reducing cardioembolic strokes compared with aspirin (HR, 0.57 [95% CI, 0.31-1.03]; P?=?.06) but was not associated with reducing other stroke subtypes.
Conclusions and Relevance:
For patients with systemic atherosclerosis, low-dose rivaroxaban plus aspirin was associated with large, significant reductions in cardioembolic strokes and embolic strokes of undetermined source. However, these results of exploratory analysis need to be independently confirmed before influencing clinical practice.
Trial Registration:
ClinicalTrials.gov identifier: NCT01776424.
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