Aortic stiffness is not only associated with structural but also functional parameters of retinal microcirculation.

OBJECTIVE: The aim of the study was to test the hypothesis that alterations in large arteries are associated with microvascular remodelling and decreased retinal capillary blood flow. METHODS: The study group comprised of 88 patients with essential hypertension and 32 healthy controls. Retinal microcirculation was evaluated by scanning laser Doppler flowmetry. Macrovascular changes were assessed on the basis of arterial stiffness measurement (carotid-femoral pulse wave velocity), its hemodynamic consequences (central pulse pressure, augmentation pressure, augmentation index) and intima media thickness of common carotid artery. RESULTS: Pulse wave velocity was inversely correlated to mean retinal capillary blood flow in hypertensive patients (R = -0.32, p < 0.01). This relationship remained significant in multivariate regression analysis after adjustment for age, sex, central systolic blood pressure (BP) and body mass index (ß = -31.27, p < 0.001). Lumen diameter (LD) of retinal arterioles was significantly smaller in hypertensive then normotensive subjects (79.4 vs. 83.8, p = 0.03). Central and brachial systolic, diastolic and mean BPs were significantly correlated with LD and outer diameter of retinal arterioles. The relationship between LD and central BPs remained significant in multivariate analysis (ß = -0.15, p = 0.03 for cSBP; ß = -0.22, p = 0.04 for cDBP; ß = -0.21, p = 0.03 for cMBP). Moreover, in a subgroup with cardiac damage central and brachial pulse pressure were positively associated with retinal wall thickness, wall cross sectional area, and wall to lumen ratio. CONCLUSION: In conclusion, the study provides a strong evidence that microcirculation is coupled with macrocirculation not only in terms of structural but also functional parameters.

Lumen narrowing and increased wall to lumen ratio of retinal microcirculation are valuable biomarkers of hypertension-mediated cardiac damage.

Purpose: In the course of hypertension, left ventricular hypertrophy and diastolic dysfunction develop very often and may progress toward heart failure. The aim of the study was to analyze the relationship between abnormalities of retinal microcirculation and cardiac damage defined as left ventricular hypertrophy and/or diastolic dysfunction.Materials and methods: The study comprised 88 patients with essential hypertension. The group was divided into two subgroups: hypertensives without cardiac damage (n = 55) and with cardiac damage (n = 33). Control group comprised 32 normotensive subjects. Scanning laser Doppler flowmetry was used to evaluate retinal microcirculation. Echocardiography was used to assess cardiac damage.Results: Lumen diameter of retinal arterioles was significantly smaller in patients with cardiac damage vs. controls (77 vs. 84 µm, p = 0.02). Additionally, there was an evident trend with respect to lumen diameter (LD) across all three studied subgroups; i.e.: the smallest dimeters were present in cardiac damage patients, moderate size in hypertensives' without cardiac damage, and the largest diameters in healthy controls (pfor trend < 0.01). Lumen diameter was inversely correlated with cardiac intraventricular septum diameter (R = -0.25, p = 0.02), left ventricular mass (R = -0.24, p = 0.02), and left atrial volume (R = -0.22, p = 0.04). Wall to lumen ratio was associated with intraventricular septum diameter (R = 0.21, p = 0.044) and left atrial volume (R = 0.21, p = 0.045). In multivariable regression analysis, lumen diameter was independently associated with intraventricular septum diameter (ß = -0.05, p = 0.03), left ventricular mass (ß = -1.15, p = 0.04), and left atrial volume (ß = -0.42, p = 0.047); wall to lumen ratio was independently associated with intraventricular septum diameter (ß = 3.67, p = 0.02) and left atrial volume (ß = 30.0, p = 0.04).Conclusions: In conclusion, retinal arterioles lumen diameter and wall to lumen ratio were independent biomarkers of cardiac damage. Retinal examination performed by means of scanning laser Doppler flowmetry might be a valuable tool to improve cardiovascular risk stratification of hypertensive patients.

Prevalence and distribution of left ventricular diastolic dysfunction in treated patients with long-lasting hypertension.

BACKGROUND: Although the presence of sub-clinical left ventricular diastolic dysfunction (LVDD) increases cardiovascular risk, the current ESH/ESC guidelines do not include the presence of this condition in the list of target organ damage or cardiovascular risk charts dedicated to the hypertensive population. Several conditions may predict the LVDD occurrence, however, clustering of these factors with hypertension makes the relationship less clear. Therefore, the aim of this study was to evaluate both the occurrence and the severity of diastolic dysfunction in a large cohort of treated hypertensives. METHODS: We retrospectively analyzed records of 610 hypertensive participants of the CARE NORTH Study who consented to echocardiography and were free of overt cardiovascular disease. Mean age was 54.0 ± 13.9 years (mean ± SD), BMI 29.7 ± 4.8 kg/m2. The exclusion criteria were: established heart failure, LVEF <45%, coronary revascularization, valvular defect, atrial fibrillation, or stroke. The staging of LVDD was based on comprehensive transthoracic echocardiographic measurements. RESULTS: 49.7% percent of the patients had normal diastolic function (38.8% vs. 59.0%, females (F) vs. males (M), respectively; p < .001). Grade 1 LVDD was documented in 24.4% (27.8% and 21.6%; F and M; p = .08) and grade 2 LVDD in 19.3% (24.9% and 14.6%; F and M; p = .001) of the patients. None were diagnosed with grade 3 LVDD. In the logistic regression model, female sex, advancing age, obesity status, established diabetes mellitus, higher 24-hour SBP, and increasing LVMI were identified as the independent variables increasing the odds for the presence of LVDD, whereas blood-lowering therapy attenuated the risk. CONCLUSIONS: There is an unexpectedly high prevalence of different forms of diastolic dysfunction in treated hypertensive patients who are free of overt cardiovascular disease.

Is the 2016 ESC diagnostic algorithm useful for assessing the prevalence of chronic heart failure in population-based studies?

BACKGROUND: Chronic heart failure (CHF) is a major healthcare problem. However, there are no epidemiological studies assessing the prevalence of CHF in the general population with diagnosis based on algorithms recommended for clinical practice. AIM: The aim of the HF-Pomorskie survey was to assess the prevalence of three basic components of the 2016 ESC diagnostic algorithm for CHF (symptoms, N-terminal pro B-type natriuretic peptide [NT-proBNP], and abnormalities on echocardiography) and to determine whether this algorithm may be applicable to studies in general population samples. METHODS: The study was performed in a representative sample of 313 adults (170 women and 143 men) aged between 20 and 90 years (mean 55.2 years [15.3]) in Northern Poland. A questionnaire to determine New York Heart Association [NYHA] class, laboratory tests including NT-proBNP, as well as transthoracic echocardiography and spirometry examinations were performed in all subjects. RESULTS: Dyspnea (NYHA class II-IV) was reported by 13.7% of recruited participants. Dyspnea and elevated levels of NT-proBNP (>125 pg/ml) were found in 7.7% of all examined subjects, while dyspnea, elevated NT-proBNP levels accompanied by systolic or diastolic abnormalities on echocardiography occurred in 4.8%. In the group without dyspnea (86.3% of all examined subjects), every sixth subject had an elevated level of NT-proBNP. On the other hand, 5.8% of studied subjects reported a previous diagnosis of CHF, which was confirmed using the current ESC algorithm in 78% of them. CONCLUSIONS: The prevalence of CHF assessed by the 2016 ESC diagnostic algorithm in the representative sample of adults was equal to 4.8%. The clinical algorithm for the diagnosis of CHF is fully applicable to the representative surveys in the general population. However, due to logistic and economic factors, echocardiography examination and NT-proBNP determination can be limited to patients reporting dyspnea or previous diagnosis of CHF.

Intima-media thickness in patients with obstructive sleep apnea without comorbidities.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with elevated risk of cardiovascular events. The early stages of vascular complications can be visualized by means of ultrasound. Intima-media thickness (IMT) correlates with the presence of risk factors of cardiovascular diseases such as hypertension, diabetes, tobacco smoking, or hyperlipidemia. However, little is known whether OSA itself may be the cause of IMT thickening. METHODS: The study group was composed of 28 patients (6 women, 22 men; mean age = 53.8 years, mean BMI = 27.1 kg/m(2), mean AHI = 22.4/h) with OSA who had no comorbidities. The control group consisted of 28 healthy subjects (6 women, 22 men; mean age = 53.9 years; mean BMI = 27.5 kg/m(2)). In both groups IMT was assessed in common carotid arteries with the use of ultrasonography. Additionally, in patients with OSA, pulse wave velocity, echocardiography, 24-h automated blood pressure monitoring, clinical signs and symptoms, and blood tests were performed to investigate possible correlations with IMT. RESULTS: Median IMT was 0.41 mm in OSA patients and 0.46 mm in the control group (p = 0.087). Echocardiography revealed left ventricle hypertrophy in 21%, systolic disorders in 8%, and diastolic disorders in 57% of the patients. In a large majority of patients, pulse wave velocity was found to be normal. IMT correlated with age (r = 0.446, p = 0.017), total cholesterol (r = 0.518, p = 0.005), daytime systolic blood pressure (r = 0.422, p = 0.025), pulse pressure 24 h and daytime (r = 0.424, p = 0.027 and r = 0.449, p = 0.019), early mitral flow/atrial mitral flow (E/A) (r = -0.429, p = 0.023), and posterior wall diameter (PWD) (r = 0.417, p = 0.270). CONCLUSION: In a relatively nonobese group of patients, no significant differences were found in the intima-media thickness between OSA patients without concomitant cardiovascular diseases and healthy controls. This may lead to the conclusion that IMT does not reflect increased risk of cardiovascular events in patients with isolated OSA.

Autonomous Aldosterone Secretion in Patients with Adrenal Incidentaloma.

In recent years, research has emphasized the significance of mild clinical and biochemical presentations of primary aldosteronism (PA) that do not meet current diagnostic criteria of the syndrome. In this study, we assessed the prevalence of autonomous aldosterone (Ald) secretion (AAS), defined as a positive (>1.2 ng/dL/mIU/L) Ald-to-renin ratio (ADRR) combined with unsuppressed Ald (>4 ng/dL), and its associations with blood pressure (BP), cardiac function, and common carotid artery (CCA) intima-media thickness (IMT) in patients with incidentally discovered adrenal adenomas (AI), who were either normo- or hypertensive but had no other cardiovascular disease. Among 332 AI patients hospitalized between November 2018 and December 2019, 63 study participants were recruited (26 normo- and 37 hypertensive), who underwent hormonal examinations, 24 h ambulatory BP measurement, transthoracic echocardiography, and CCA IMT assessment without altering chronic medications. AAS was found in approximately 25% of subjects (seven normo- and nine hypertensive); urinary aldosterone excretion (UAldE) exceeded 10 ug/day in none of the subjects. The left ventricular mass index correlated positively with UAldE in non-diabetic patients (n = 50), and negatively with renin in those without beta blocker therapy (n = 38). The study shows that a pragmatic approach to hormonal assessment (no chronic therapy modification) may reveal patients with AAS. Screening for this subclinical PA presentation is probably more effective with a permissive ADRR than UAldE in such a setting.

Increased inspiratory resistance affects the dynamic relationship between blood pressure changes and subarachnoid space width oscillations.

BACKGROUND AND OBJECTIVE: Respiration is known to affect cerebrospinal fluid (CSF) movement. We hypothesised that increased inspiratory resistance would affect the dynamic relationship between blood pressure (BP) changes and subarachnoid space width (SAS) oscillations. METHODS: Experiments were performed in a group of 20 healthy volunteers undergoing controlled intermittent Mueller Manoeuvres (the key characteristic of the procedure is that a studied person is subjected to a controlled, increased inspiratory resistance which results in marked potentiation of the intrathoracic negative pressure). BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography; oxyhaemoglobin saturation with an ear-clip sensor; end-tidal CO2 with a gas analyser; cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a new method i.e. near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the BP and SAS oscillations coupling. RESULTS: Initiating Mueller manoeuvres evoked cardiac SAS component decline (-17.8%, P<0.001), systolic BP, diastolic BP and HR increase (+6.3%, P<0.001; 6.7%, P<0.001 and +2.3%, P<0.05, respectively). By the end of Mueller manoeuvres, cardiac SAS component and HR did not change (+2.3% and 0.0%, respectively; both not statistically significant), but systolic and diastolic BP was elevated (+12.6% and +8.9%, respectively; both P<0.001). With reference to baseline values there was an evident decrease in wavelet coherence between BP and SAS oscillations at cardiac frequency in the first half of the Mueller manoeuvres (-32.3%, P<0.05 for left hemisphere and -46.0%, P<0.01 for right hemisphere) which was followed by subsequent normalization at end of the procedure (+3.1% for left hemisphere and +23.1% for right hemisphere; both not statistically significant). CONCLUSIONS: Increased inspiratory resistance is associated with swings in the cardiac contribution to the dynamic relationship between BP and SAS oscillations. Impaired cardiac performance reported in Mueller manoeuvres may influence the pattern of cerebrospinal fluid pulsatility.

Acute hypoxia diminishes the relationship between blood pressure and subarachnoid space width oscillations at the human cardiac frequency.

BACKGROUND: Acute hypoxia exerts strong effects on the cardiovascular system. Heart-generated pulsatile cerebrospinal fluid motion is recognised as a key factor ensuring brain homeostasis. We aimed to assess changes in heart-generated coupling between blood pressure (BP) and subarachnoid space width (SAS) oscillations during hypoxic exposure. METHODS: Twenty participants were subjected to a controlled decrease in oxygen saturation (SaO2 = 80%) for five minutes. BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography, oxyhaemoglobin saturation with an ear-clip sensor, end-tidal CO2 with a gas analyser, and cerebral blood flow velocity (CBFV), pulsatility and resistive indices with Doppler ultrasound. Changes in SAS were recorded with a recently-developed method called near-infrared transillumination/backscattering sounding. Wavelet transform analysis was used to assess the relationship between BP and SAS oscillations. RESULTS: Gradual increases in systolic, diastolic BP and HR were observed immediately after the initiation of hypoxic challenge (at fifth minute +20.1%, +10.2%, +16.5% vs. baseline, respectively; all P<0.01), whereas SAS remained intact (P = NS). Concurrently, the CBFV was stable throughout the procedure, with the only increase observed in the last two minutes of deoxygenation (at the fifth minute +6.8% vs. baseline, P<0.05). The cardiac contribution to the relationship between BP and SAS oscillations diminished immediately after exposure to hypoxia (at the fifth minute, right hemisphere -27.7% and left hemisphere -26.3% vs. baseline; both P<0.05). Wavelet phase coherence did not change throughout the experiment (P = NS). CONCLUSIONS: Cerebral haemodynamics seem to be relatively stable during short exposure to normobaric hypoxia. Hypoxia attenuates heart-generated BP SAS coupling.

Pial artery and subarachnoid width response to apnoea in normal humans.

BACKGROUND: Little is known about intracranial pressure (ICP)-cerebral haemodynamic interplay during repetitive apnoea. A recently developed method based on near-infrared transillumination/backscattering sounding (NIR-T/BSS) noninvasively measures changes in pial artery pulsation (cc-TQ) as well as subarachnoid width (sas-TQ) in humans. METHOD: We tested the complex response of the pial artery and subarachnoid width to apnoea using this method. The pial artery and subarachnoid width response to consecutive apnoeas lasting 30, 60 s and maximal breath-hold (91.1 ±â€Š23.1 s) were studied in 20 healthy volunteers. The cc-TQ and sas-TQ were measured using NIR-T/BSS; cerebral blood flow velocity (CBFV), pulsatility index and resistive index were measured using Doppler ultrasound of the left internal carotid artery; heart rate (HR) and beat-to-beat SBP and DBP blood pressure were recorded using a Finometer; end-tidal CO2 (EtCO2) was measured using a medical gas analyser. RESULTS: Apnoea evoked a multiphasic response in blood pressure, pial artery compliance and ICP. First, SBP declined, which was accompanied by an increase in cc-TQ and sas-TQ. Directly after these changes, SBP exceeded baseline values, which was followed by a decline in cc-TQ and the return of sas-TQ to baseline. During these initial changes, CBFV remained stable. Towards the end of the apnoea, BP, cc-TQ and CBFV increased, whereas pulsatility index, resistive index and sas-TQ declined. Changes in sas-TQ were linked to changes in EtCO2, HR and SBP. CONCLUSION: Apnoea is associated with ICP swings, closely reflecting changes in EtCO2, HR and peripheral BP. The baroreflex influences the pial artery response.

Tissue Doppler indexes of left ventricular systolic function in relation to the pulsatile and steady components of blood pressure in a general population.

OBJECTIVES: To our knowledge, no population study described the association of the radial and longitudinal components of left ventricular strain with blood pressure (BP) components in continuous analyses. We therefore investigated these associations in participants randomly recruited from the general population in the framework of the family-based European Project on Genes in Hypertension. METHODS: In 334 participants (55.4% women; mean age, 43.6 year), using tissue Doppler imaging (TDI), we measured the end-systolic longitudinal strain (mean 20.9%) and peak systolic strain rate (1.29 s) from the basal portion of the left ventricular inferior and posterior free walls and radial stain (51.1%) and strain rate (3.40 s) of the left ventricular posterior wall. Models included in addition to covariables and confounders both SBP and DBP or both pulse pressure (PP) and mean arterial pressure (MAP). Effect sizes were expressed per 1-SD increase in BP. RESULTS: Longitudinal strain (-0.62%; P = 0.04 and -0.64%; P = 0.007), but not strain rate, decreased with DBP and MAP. Radial strain (4.0 and -3.4%; P ≤ 0.001) and strain rate (0.38 and -0.18 s; P ≤ 0.04) independently increased with SBP and decreased with DBP. Accordingly, radial strain (2.9%; P < 0.0001) and strain rate (0.22 s; P = 0.0005) increased with higher PP, but were not related to MAP. CONCLUSION: In the general population, BP is an independent determinant of left ventricular systolic function as measured by TDI. Radial function increased with PP, the pulsatile BP component, whereas longitudinal function decreased with the steady component of BP as expressed by MAP or DBP.

An independent relationship between muscle sympathetic nerve activity and pulse wave velocity in normal humans.

OBJECTIVE: Carotid-femoral pulse wave velocity (PWV) has been shown to be a powerful predictor of cardiovascular morbidity and mortality. Sympathetic neural mechanisms may have a stiffening influence on arterial mechanical properties. The relationship between direct measures of sympathetic traffic and PWV in healthy humans has not been previously studied. We, therefore, tested the hypothesis that PWV is independently linked to muscle sympathetic nerve activity (MSNA) in normal individuals. METHODS: We measured MSNA (microneurography), PWV (Complior device), heart rate and blood pressure in 25 healthy male participants (mean age 43 +/- 10 years). RESULTS: PWV correlated significantly with age (r = 0.63, P < 0.001), SBP (r = 0.43, P < 0.05) and MSNA (r = 0.43, P < 0.05) but not with BMI, waist circumference, waist-to-hip ratio, heart rate, pulse pressure or DBP. Robust multiple linear regression analysis revealed that only age and MSNA were linked independently to PWV (r2 = 0.62, P < 0.001), explaining 39 and 25% of its variance, respectively. After adjustment of PWV for age and SBP, we further divided individuals into 'excessive' PWV (i.e. higher than expected from age and SBP) and 'optimal' PWV (i.e. lower than expected). BMI and blood pressure were similar in both subgroups. Individuals with excessive PWV had significantly greater MSNA than individuals with optimal PWV (30 +/- 10 vs. 18 +/- 11 bursts/min, P = 0.01). CONCLUSION: This study provides the first evidence that PWV is linked to MSNA in normal humans. The relationship between MSNA and PWV is independent of age, BMI, waist circumference, waist-to-hip ratio, heart rate, pulse pressure or blood pressure.

Cerebrovascular reactivity, intima-media thickness, and nephropathy presence in patients with type 1 diabetes.

OBJECTIVE: Cerebrovascular reactivity impairment was reported as a marker of cerebral microangiopathy in long-term type 1 diabetes. Intima-media complex thickening reflects early stages of macroangiopathy in type 1 diabetes. The analysis of the relationship between these variables and other microangiopathic complications might serve as a beneficial indicator for early prophylaxis in these patients. RESEARCH DESIGN AND METHODS: Vasomotor reactivity reserve (VMRr) and breath-holding index (BHI) of the middle cerebral artery were measured with transcranial Doppler in 59 patients (median age 32.0 years, range 20-51, 36 females) with type 1 diabetes, without history of cerebrovascular events, and 30 healthy control subjects (median age 31.5 years, range 25-39, 15 females). The relationships between the presence of selected vascular complications of type 1 diabetes and biochemical parameters, intima-media thickness (IMT), and VMRr and BHI in patients were analyzed. RESULTS: VMRr and BHI were lower in patients with type 1 diabetes when compared with healthy subjects (81.5 vs. 100%, P < 0.01, and 1.6 vs. 2.2, P = 0.04, respectively), whereas IMT was significantly higher in patients then in healthy control subjects (0.36 vs. 0.30 mm, P = 0.001). However, no association of IMT with VMRr was found. We found a significant reduction of VMRr and BHI in patients with diabetic nephropathy. CONCLUSIONS: The presence of diabetic nephropathy, but not IMT, can be regarded as an indicator of cerebral microangiopathy severity in patients with type 1 diabetes.