Cuffless Blood Pressure Measurement.

Cuffless blood pressure (BP) measurement has become a popular field due to clinical need and technological opportunity. However, no method has been broadly accepted hitherto. The objective of this review is to accelerate progress in the development and application of cuffless BP measurement methods. We begin by describing the principles of conventional BP measurement, outstanding hypertension/hypotension problems that could be addressed with cuffless methods, and recent technological advances, including smartphone proliferation and wearable sensing, that are driving the field. We then present all major cuffless methods under investigation, including their current evidence. Our presentation includes calibrated methods (i.e., pulse transit time, pulse wave analysis, and facial video processing) and uncalibrated methods (i.e., cuffless oscillometry, ultrasound, and volume control). The calibrated methods can offer convenience advantages, whereas the uncalibrated methods do not require periodic cuff device usage or demographic inputs. We conclude by summarizing the field and highlighting potentially useful future research directions.

The prevalence and impact of orthostatic intolerance in young women across the hypermobility spectrum.

Orthostatic intolerance (OI) is frequently reported in young women with generalized hypermobility spectrum disorder (G-HSD) and hypermobile EDS (hEDS). However, it remains currently unclear whether OI is a comorbidity or fundamental part of the pathophysiology of G-HSD or hEDS. This study investigated the prevalence and impact of OI in young women across the hypermobility spectrum. Forty-five women (14-30 years, 15 controls, 15 G-HSD, and 15 hEDS) undertook a head-up tilt (HUT) and active stand test. Postural Orthostatic Tachycardia Syndrome (POTS) and Orthostatic Hypotension (OH) were assessed using age-related criteria. Autonomic dysfunction and quality-of-life questionnaires were also completed. The prevalence of POTS was higher in women with G-HSD than hEDS and control groups during HUT (43% vs. 7% and 7%, respectively, p < 0.05), but similar between groups during the active stand (47%, 27%, and 13% for G-HSD, hEDS, and control, respectively). No participants had OH. hEDS and G-HSD participants reported more severe orthostatic symptoms and poorer quality of life than controls. Although POTS was observed in hypermobile participants, there is no conclusive evidence that its prevalence differed between groups due to differences between the HUT and active stand assessments. Nevertheless, OI and broader autonomic dysfunction impacted on their quality of life.

Measuring Arterial Stiffness in Animal Experimental Studies.

The arterial wall is a composite material of elastin, collagen, and extracellular matrix with acutely modifiable material properties through the action of smooth muscle cells. Therefore, arterial stiffness is a complex parameter that changes not only with long-term remodeling of the wall constituents but also with acute contraction or relaxation of smooth muscle or with changes in the acute distending pressure to which the artery is exposed. It is not possible to test all these aspects using noninvasive or even invasive techniques in humans. Full characterization of the mechanical properties of the artery and the specific arterial factors causing changes to stiffness with disease or modified lifestyle currently require animal studies. This article summarizes the major in vivo and ex vivo techniques to measure the different aspects of arterial stiffness in animal studies.

Reply to Comments: Using the Cardio-Ankle Vascular Index (CAVI) or the Mathematical Correction Form (CAVI0) in Clinical Practice.

We read with great interest Alizargar et al [...].

Mechanism underlying the heart rate dependency of wave reflection in the aorta: a numerical simulation.

Arterial wave reflection has been shown to have a significant dependence on heart rate (HR). However, the underlying mechanisms inherent in the HR dependency of wave reflection have not been well established. This study aimed to investigate the potential mechanisms and role of arterial viscoelasticity using a 55-segment transmission line model of the human arterial tree combined with a fractional viscoelastic model. At varying degrees of viscoelasticity modeled as fractional order parameter α, reflection magnitude (RM), reflection index (RI), augmentation index (AIx), and a proposed novel normalized reflection coefficient (Γnorm) were estimated at different HRs from 60 to 100 beats/min with a constant mean flow of 70 ml/s. RM, RI, AIx, and Γnorm at the ascending aorta decreased linearly with increasing HR at all degrees of viscoelasticity. The means ± SD of the HR dependencies of RM, RI, AIx, and Γnorm were -0.042 ± 0.004, -0.018 ± 0.001, -1.93 ± 0.55%, and -0.037 ± 0.002 per 10 beats/min, respectively. There was a significant and nonlinear reduction in RM, RI, and Γnorm with increasing α at all HRs. In addition, HR and α have a more pronounced effect on wave reflection at the aorta than at peripheral arteries. The potential mechanism of the HR dependency of wave reflection was explained by the inverse dependency of the reflection coefficient on frequency, with the harmonics of the pulse waveform moving toward higher frequencies with increasing HR. This HR dependency can be modulated by arterial viscoelasticity. NEW & NOTEWORTHY This in silico study addressed the underlying mechanisms of how heart rate influences arterial wave reflection based on a transmission line model and elucidated the role of arterial viscoelasticity in the dependency of arterial wave reflection on heart rate. This study provides insights into wave reflection as a frequency-dependent phenomenon and demonstrates the validity of using reflection magnitude and reflection index as wave reflection indexes.

Arterial Flow, Pulse Pressure and Pulse Wave Velocity in Men and Women at Various Ages.

The increase in pulse pressure (PP) that occurs with advancing age is predominantly due to reduced arterial distensibility leading to decreased aortic compliance, particularly in the elderly, in whom high blood pressure mainly manifests as isolated systolic hypertension. Since age-related changes in stroke volume are minimal compared with changes in PP, PP is often considered a surrogate measure of arterial stiffness. However, since PP is determined by both cardiac and arterial function, a more precise and reliable means of assessment of arterial stiffness is arterial pulse wave velocity (PWV), a parameter that is only dependent on arterial properties. Arterial stiffness as measured by PWV has been found to be a powerful pressure-related indicator for cardiovascular morbidity and mortality. We analyzed PP and PWV in men and women of various age groups in healthy volunteers as well as cardiac patients with different types of diseases. The findings identified several striking sex-specific differences which demand consideration in guidelines for diagnostic procedures, for epidemiological analysis, and in evaluation of therapeutic interventions.

Arterial viscoelasticity: role in the dependency of pulse wave velocity on heart rate in conduit arteries.

Experimental investigations have established that the stiffness of large arteries has a dependency on acute heart rate (HR) changes. However, the possible underlying mechanisms inherent in this HR dependency have not been well established. This study aimed to explore a plausible viscoelastic mechanism by which HR exerts an influence on arterial stiffness. A multisegment transmission line model of the human arterial tree incorporating fractional viscoelastic components in each segment was used to investigate the effect of varying fractional order parameter (α) of viscoelasticity on the dependence of aortic arch to femoral artery pulse wave velocity (afPWV) on HR. HR was varied from 60 to 100 beats/min at a fixed mean flow of 100 ml/s. PWV was calculated by intersecting tangent method (afPWVTan) and by phase velocity from the transfer function (afPWVTF) in the time and frequency domain, respectively. PWV was significantly and positively associated with HR for α ≥ 0.6; for α = 0.6, 0.8, and 1, HR-dependent changes in afPWVTan were 0.01 ± 0.02, 0.07 ± 0.04, and 0.22 ± 0.09 m/s per 5 beats/min; HR-dependent changes in afPWVTF were 0.02 ± 0.01, 0.12 ± 0.00, and 0.34 ± 0.01 m/s per 5 beats/min, respectively. This crosses the range of previous physiological studies where the dependence of PWV on HR was found to be between 0.08 and 0.10 m/s per 5 beats/min. Therefore, viscoelasticity of the arterial wall could contribute to mechanisms through which large artery stiffness changes with changing HR. Physiological studies are required to confirm this mechanism.NEW & NOTEWORTHY This study used a transmission line model to elucidate the role of arterial viscoelasticity in the dependency of pulse wave velocity on heart rate. The model uses fractional viscoelasticity concepts, which provided novel insights into arterial hemodynamics. This study also provides a means of assessing the clinical manifestation of the association of pulse wave velocity and heart rate.

Improved assessment of arterial stiffness using corrected cardio-ankle vascular index (CAVI0) in overweight adolescents with white-coat and essential hypertension.

Arterial stiffness is a marker of vascular damage. Although adiposity increases cardiovascular risk, the relationship between paediatric overweight and arterial stiffness is unclear. The study aimed to evaluate the simultaneous effect of hypertension and overweight on arterial stiffness using cardio-ankle vascular index (CAVI) and related novel, theoretically blood pressure (BP)-independent, index CAVI0. CAVI and CAVI0 were measured in 140 adolescent boys (16.0 ± 1.9 years) divided into age-matched groups: normal-weight normotensives, overweight normotensives, overweight white-coat hypertensives, and overweight essential hypertensives. Overweight normotensives had significantly lower CAVI and CAVI0 compared to normal-weight normotensives (4.81 ± 0.64 vs. 5.33 ± 0.66, p < .01; 7.10 ± 0.99 vs. 7.81 ± 1.00, p < .01, respectively). CAVI and CAVI0 in overweight essential hypertensives showed no significant difference compared to normal-weight normotensives and were significantly higher compared to overweight normotensives (5.32 ± 0.77 vs. 4.81 ± 0.64, p < .01; 7.77 ± 1.19 vs. 7.10 ± 0.99, p < .01, respectively). CAVI, but not CAVI0, was associated positively with diastolic pressure (0.022 mmHg-1, p = .002) and negatively with pulse pressure (-0.022 mmHg-1, p = .001), and it was significantly higher in overweight white-coat hypertensives compared to overweight normotensives (5.20 ± 0.63 vs. 4.81 ± 0.64, p < .05). The lowering effect of overweight on arterial stiffness indexed by CAVI and CAVI0 in hypertensive adolescents seems to counterbalance the early arteriosclerotic effect of essential hypertension. The increase in CAVI, but not CAVI0, in overweight white-coat hypertensives could be attributable to residual BP dependence of CAVI, which is not present in CAVI0. Under certain conditions, CAVI0 may offer a clinically relevant improved assessment of arterial stiffness superior to CAVI.

Long-Term Angiotensin II Receptor Blockade Limits Hypertension, Aortic Dysfunction, and Structural Remodeling in a Rat Model of Chronic Kidney Disease.

BACKGROUND/AIMS: Chronic kidney disease (CKD) is associated with large artery remodeling, endothelial dysfunction and calcification, with angiotensin II (Ang II) a known driver of these pathologies. We investigated long-term Ang II type 1 receptor inhibition with valsartan on aortic function and structure in the Lewis polycystic kidney (LPK) rat model of CKD. METHODS: Mixed sex LPK and Lewis control (total n = 28) treated (valsartan 60 mg/kg/day p.o. from 4 to 18 weeks) and vehicle groups were studied. Functional responses to noradrenaline (NA), potassium chloride and endothelium-dependent and independent relaxations were investigated in vitro using acetylcholine hydrochloride (ACh) and sodium nitroprusside (SNP), respectively. Effects of the nitric oxide synthase (NOS) substrate L-arginine, NOS inhibitor L-NAME and cyclooxygenase inhibitor indomethacin on ACh responses were examined. RESULTS: In the LPK, valsartan reduced systolic blood pressure and urinary protein, ameliorated exaggerated sensitivity to NA, and normalized endothelium-dependent (ACh-Rmax; 91 ± 7 vs. 59 ± 6%, p = 0.0001) and independent dysfunction (SNP-Rmax; 99 ± 1 vs. 82 ± 7%, p = 0.040), as well as improving NO-dependent relaxation (Rmax; -51 ± 6 vs. -26 ± 9%, p = 0.008). Valsartan also reduced aortic wall hypertrophy, elastin disruption/fragmentation, calcification, media cystic degeneration, and levels of matrix metalloproteinase 9. CONCLUSIONS: This study highlights the role of Ang II in driving vascular manifestations of CKD and indicates that early treatment can significantly limit pathological changes.

Central Pulsatile Pressure and Flow Relationship in the Time and Frequency Domain to Characterise Hydraulic Input to the Brain and Cerebral Vascular Impedance.

In the time domain, pulsatile flow and pressure can be characterised as the ratio of the late systolic boost of flow or pressure to the pulse amplitude so as to estimate the hydraulic input to the brain. While vascular impedance has been widely used to represent the load presented to the heart by the systemic circulation, it has not been applied to the cerebral circulation.We set out to study the relationship between the pressure and the flow augmentation index (AIx) in the time domain and to determine cerebral vascular impedance using aortic blood pressure and cerebral blood flow waveforms in the frequency domain. Twenty-four young subjects (aged 21-39 years) were recruited; aortic pressure was derived using SphygmoCor from radial pressure. Flow waveforms were recorded from the middle cerebral artery. In three subjects, we performed the Valsalva manoeuvre to investigate their response to physiological intervention. There was a linear relationship between flow and pressure AIx, and cerebral impedance values were similar to those estimated for low resistance vascular beds. Substantial change in pressure and flow wave contour was observed during the Valsalva manoeuvre; however, the relationship in both the time and the frequency domains were unchanged. This confirms that aortic pressure and cerebral flow waveform can be used to study cerebral impedance.

Intracranial Pressure Waveforms are More Closely Related to Central Aortic than Radial Pressure Waveforms: Implications for Pathophysiology and Therapy.

In patients with subarachnoid haemorrhage, pulsatile intracranial pressure (ICP) is more strongly associated with adverse events than mean ICP. Furthermore, patients with idiopathic normal-pressure hydrocephalus (iNPH), and pulsatile ICP of 5 mmHg or more, gain more benefit from cerebrospinal fluid (CSF) shunting than those whose pulsatile ICP is lower than 5 mmHg.Our study aims to investigate the morphological relationship between ICP pulsations, aortic pressure pulsations and radial artery pulsations. Central aortic pulse pressure has been known to be the best predictor of adverse cardiac events, whereas radial artery pulse pressure is generally measured and displayed in intensive care environments.We studied 10 patients with iNPH, and their ICP and aortic and radial pressures were digitised, ensemble-averaged and compared in the time and frequency domains. The ICP wave contour was quite different to the radial pressure waveform. By contrast, the ICP waveform was similar to the aortic pressure wave contour. The ICP amplitude averaged <10 % of aortic pulse pressure. In the frequency domain, the relative amplitude of the first three harmonics was similar for the ICP and aortic pressure. Hence, monitoring central aortic pressure through derivation from the radial pressure wave is superior to measurement of radial pressure alone.

Change in Pulsatile Cerebral Arterial Pressure and Flow Waves as a Therapeutic Strategy?

While intracranial pressure (ICP), arterial pressure and transcranial middle cerebral artery flow velocity (MCAFV) are often monitored in unconscious patients following stroke or head injury, the value of waveform indices has not been fully established. We retrospectively analysed the data of eight adults (aged 19-36 years) with closed head injury who had spontaneous and repeated episodes of elevated ICP (i.e. "plateau waves"). MCAFV was measured using transcranial Doppler, ICP using a Codman catheter and radial artery pressure using cannulation. Ascending aortic pressure (AAP) was generated from the radial artery using SphygmoCor(TM). Cerebral perfusion pressure (CPP) was calculated as AAP - ICP in the time domain.During the period of increased ICP, ICP and cerebral flow velocity amplitude increased significantly compared with the basal condition, while cerebral mean flow decreased. Amplitude of the secondary peak in ICP, AAP and MCAFV waveform became apparent.An increase in the amplitude of ICP, AAP and MCAFV waves can be attributed to the greater prominence of reflected waves from the lower body, which was apparent in pulse waveform analysis. Arterial vasodilators such as nitrates reduce reflected pressure waves from the lower body and, by decreasing the amplitude of AAP, ICP and MCAFV, may be as beneficial for the cerebral circulation as they are for the left ventricle of the heart.

Does Replacing Sodium Excreted in Sweat Attenuate the Health Benefits of Physical Activity?

International guidelines suggest limiting sodium intake to 86-100 mmol/day, but average intake exceeds 150 mmol/day. Participants in physical activities are, however, advised to increase sodium intake before, during and after exercise to ensure euhydration, replace sodium lost in sweat, speed rehydration and maintain performance. A similar range of health benefits is attributable to exercise and to reduction in sodium intake, including reductions in blood pressure (BP) and the increase of BP with age, reduced risk of stroke and other cardiovascular diseases, and reduced risk of osteoporosis and dementia. Sweat typically contains 40-60 mmol/L of sodium, leading to approximately 20-90 mmol of sodium lost in one exercise session with sweat rates of 0.5-1.5 L/h. Reductions in sodium intake of 20-90 mmol/day have been associated with substantial health benefits. Homeostatic systems reduce sweat sodium as low as 3-10 mmol/L to prevent excessive sodium loss. "Salty sweaters" may be individuals with high sodium intake who perpetuate their "salty sweat" condition by continual replacement of sodium excreted in sweat. Studies of prolonged high intensity exercise in hot environments suggest that sodium supplementation is not necessary to prevent hyponatremia during exercise lasting up to 6 hr. We examine the novel hypothesis that sodium excreted in sweat during physical activity offsets a significant fraction of excess dietary sodium, and hence may contribute part of the health benefits of exercise. Replacing sodium lost in sweat during exercise may improve physical performance, but may attenuate the long-term health benefits of exercise.

Pressure dependency of aortic pulse wave velocity in vivo is not affected by vasoactive substances that alter aortic wall tension ex vivo.

Aortic stiffness, a predictive parameter in cardiovascular medicine, is blood pressure dependent and experimentally requires isobaric measurement for meaningful comparison. Vasoactive drug administration to change peripheral resistance and blood pressure allows such isobaric comparison but may alter large conduit artery wall tension, directly changing aortic stiffness. This study quantifies effects of sodium nitroprusside (SNP, vasodilator) and phenylephrine (PE, vasoconstrictor) on aortic stiffness measured by aortic pulse wave velocity (aPWV) assessed by invasive pressure catheterization in anaesthetized Sprague-Dawley rats (n = 7). This was compared with nondrug-dependent alteration of blood pressure through reduced venous return induced by partial vena cava occlusion. In vivo drug concentration was estimated by modeling clearance rates. Ex vivo responses of excised thoracic and abdominal aortic rings to drugs was measured using myography. SNP administration did not alter aPWV compared with venous occlusion (P = 0.21-0.87). There was a 5% difference in aPWV with PE administration compared with venous occlusion (P < 0.05). The estimated in vivo maximum concentration of PE (7.0 ± 1.8 ×10(-7) M) and SNP (4.2 ± 0.6 ×10(-7) M) caused ex vivo equivalent contraction of 52 mmHg (thoracic) and 112 mmHg (abdominal) and relaxation of 96% (both abdominal and thoracic), respectively, despite having a negligible effect on aPWV in vivo. This study demonstrates that vasoactive drugs administered to alter systemic blood pressure have a negligible effect on aPWV and provide a useful tool to study pressure-normalized and pressure-dependent aPWV in large conduit arteries in vivo. However, similar drug concentrations affect aortic ring wall tension ex vivo. Future studies investigating in vivo and ex vivo kinetics will need to elucidate mechanisms for this marked difference.

Opposing changes in thoracic and abdominal aortic biomechanical properties in rodent models of vascular calcification and hypertension.

This study investigated the effects of hypertension on regional aortic biomechanical and structural properties in three rat models of vascular calcification: the hypertensive Lewis polycystic kidney (LPK; n = 13) model of chronic kidney disease, spontaneously hypertensive rats (SHRs; n = 12), and calcification in normotensive Lewis rats induced by vitamin D3 and nicotine (VDN; n = 8). Lewis and Wistar-Kyoto rats were controls. Thoracic and abdominal aortic stiffness parameters were assessed by tensile testing. In models where aortic stiffness differences compared with controls existed in both thoracic and abdominal segments, an additional cohort was quantified by histology for thoracic and abdominal aortic elastin, collagen, and calcification. LPK and VDN animals had higher thoracic breaking strain than control animals (P < 0.01 and P < 0.05, respectively) and lower energy absorption within the tensile curve of the abdominal aorta (P < 0.05). SHRs had a lower abdominal breaking stress than Wistar-Kyoto rats. LPK and VDN rats had more elastic lamellae fractures than control rats (P < 0.001), which were associated with calcium deposition (thoracic R = 0.37, P = 0.048; abdominal: R = 0.40, P = 0.046). LPK rats had higher nuclear density than control rats (P < 0.01), which was also evident in the thoracic but not abdominal aorta of VDN rats (P < 0.01). In LPK and VDN rats, but not in control rats, media thickness and cross-sectional area were at least 1.5-fold greater in thoracic than abdominal regions. The calcification models chronic kidney disease and induced calcification in normotension caused differences in regional aortic stiffness not seen in a genetic form of hypertension. Detrimental abdominal aortic remodeling but lower stiffness in the thoracic aorta with disease indicates possible compensatory mechanisms in the proximal aorta.

Robust aortic valve non-opening detection for different cardiac conditions.

In recent years, extensive studies have been conducted in the area of pumping state detection for implantable rotary blood pumps. However, limited studies have focused on automatically identifying the aortic valve non-opening (ANO) state despite its importance in the development of control algorithms aiming for myocardial recovery. In the present study, we investigated the performance of 14 ANO indices derived from the pump speed waveform using four different types of classifiers, including linear discriminant analysis, logistic regression, back propagation neural network, and k-nearest neighbors (KNN). Experimental measurements from four greyhounds, which take into consideration the variations in cardiac contractility, systemic vascular resistance, and total blood volume were used. By having only two indices, (i) the root mean square value, and (ii) the standard deviation, we were able to achieve an accuracy of 92.8% with the KNN classifier. Further increase of the number of indices to five for the KNN classifier increases the overall accuracy to 94.6%.

Myocardial oxygen supply and demand imbalance predicts mortality in older nursing home residents: The PARTAGE study.

BACKGROUND: A mismatch between myocardial oxygen supply and demand is the most common cause of ischemic myocardial injury in older persons. The subendocardial viability ratio (SEVR) can usefully estimate the degree of myocardial perfusion relative to left-ventricular workload. The aim of the present study was to evaluate the ability of SEVR to predict long-term mortality in the older population. Additionally, we aimed to identify the SEVR cutoff value best predicting total mortality. METHODS: This is a multicenter, longitudinal study involving a large population of individuals older than 80 years living in nursing homes. Patients with cancer, severe dementia, and very low level of autonomy were excluded from the study. Participants were monitored for 10 years. Adverse outcomes were recorded every 3 months from inclusion to the end of the study. SEVR reflects the balance between subendocardial oxygen supply and demand, and was estimated non-invasively by analyzing the carotid pressure waveform recorded by applanation arterial tonometry. RESULTS: A total of 828 people were enrolled (mean age: 87.7 ± 4.7 years, 78% female). 735 patients died within 10 years and 24 were lost to follow-up. SEVR was inversely associated with mortality at univariate Cox-regression model (risk ratio, 0.683 per unit increase in SEVR; 95% confidence interval (CI) [0.502-0.930], p = 0.015) and in a model including age, sex, body mass index, Activity of Daily Living index and Mini-Mental State Examination score (risk ratio, 0.647; 95% CI [0.472-0.930]). The lowest tertile of SEVR was associated with higher 10-years total mortality than the middle (p < 0.001) and the highest (p < 0.004) tertile. A SEVR cutoff value of 83% was identified as the best predictor of total mortality. CONCLUSIONS: SEVR may be considered as a marker of "cardiovascular frailty." An accurate non-invasive estimation of SEVR could be a useful and independent parameter to assess survival probability in very old adults. TRIAL REGISTRATION: NCT00901355, registered on ClinicalTrials.gov website.

2024 Recommendations for Validation of Noninvasive Arterial Pulse Wave Velocity Measurement Devices.

BACKGROUND: Arterial stiffness, as measured by arterial pulse wave velocity (PWV), is an established biomarker for cardiovascular risk and target-organ damage in individuals with hypertension. With the emergence of new devices for assessing PWV, it has become evident that some of these devices yield results that display significant discrepancies compared with previous devices. This discrepancy underscores the importance of comprehensive validation procedures and the need for international recommendations. METHODS: A stepwise approach utilizing the modified Delphi technique, with the involvement of key scientific societies dedicated to arterial stiffness research worldwide, was adopted to formulate, through a multidisciplinary vision, a shared approach to the validation of noninvasive arterial PWV measurement devices. RESULTS: A set of recommendations has been developed, which aim to provide guidance to clinicians, researchers, and device manufacturers regarding the validation of new PWV measurement devices. The intention behind these recommendations is to ensure that the validation process can be conducted in a rigorous and consistent manner and to promote standardization and harmonization among PWV devices, thereby facilitating their widespread adoption in clinical practice. CONCLUSIONS: It is hoped that these recommendations will encourage both users and developers of PWV measurement devices to critically evaluate and validate their technologies, ultimately leading to improved consistency and comparability of results. This, in turn, will enhance the clinical utility of PWV as a valuable tool for assessing arterial stiffness and informing cardiovascular risk stratification and management in individuals with hypertension.

Evaluation of suction detection during different pumping states in an implantable rotary blood pump.

In recent times, the problem of noninvasive suction detection for implantable rotary blood pumps has attracted substantial research interest. Here, we compare the performance of various suction indices for different types of suction and non-suction events based on pump speed irregularity. A total of 171 different indices that consist of previously proposed as well as newly introduced suction indices are tested using regularized logistic regression. These indices can be classified as amplitude based (derived from the mean, maximum, and minimum values of a cycle), duration based (derived from the duration of a cycle), gradient based (derived from the first order as well as higher order differences) and frequency based (derived from the power spectral density). The non-suction event data consists of ventricular ejection with or without arrhythmia and intermittent and continuous non-opening of the aortic valve. The suction event data consists of partial ventricular collapse that occurs intermittently as well as continuously with or without arrhythmia. In addition, we also attempted to minimize the usage of multiple indices by applying the sequential forward floating selection method to find which combination of indices gives the best performance. In general, the amplitude-based and gradient-based indices performed quite well while the duration-based and frequency-based indices performed poorly. By having only two indices ([i] the maximum gradient change in positive slope; and [ii] the standard deviation of the maximum value in a cycle), we were able to achieve a sensitivity of 98.9% and a specificity of 99.7%.