Background: The goal of this work was to create a sharable dataset of heart-driven signals, including ballistocardiograms (BCGs) and time-aligned electrocardiograms (ECGs), photoplethysmograms (PPGs), and blood pressure waveforms. Methods: A custom, bed-based ballistocardiographic system is described in detail. Affiliated cardiopulmonary signals are acquired using a GE Datex CardioCap 5 patient monitor (which collects ECG and PPG data) and a Finapres Medical Systems Finometer PRO (which provides continuous reconstructed brachial artery pressure waveforms and derived cardiovascular parameters). Results: Data were collected from 40 participants, 4 of whom had been or were currently diagnosed with a heart condition at the time they enrolled in the study. An investigation revealed that features extracted from a BCG could be used to track changes in systolic blood pressure (Pearson correlation coefficient of 0.54 +/− 0.15), dP/dt_max (Pearson correlation coefficient of 0.51 +/− 0.18), and stroke volume (Pearson correlation coefficient of 0.54 +/− 0.17). Conclusion: A collection of synchronized, heart-driven signals, including BCGs, ECGs, PPGs, and blood pressure waveforms, was acquired and made publicly available. An initial study indicated that bed-based ballistocardiography can be used to track beat-to-beat changes in systolic blood pressure and stroke volume. Significance: To the best of the authors’ knowledge, no other database that includes time-aligned ECG, PPG, BCG, and continuous blood pressure data is available to the public. This dataset could be used by other researchers for algorithm testing and development in this fast-growing field of health assessment, without requiring these individuals to invest considerable time and resources into hardware development and data collection.

Background: Cerebral small vessel disease (cSVD) is a major contributing factor to ischemic stroke and dementia. However, the vascular pathologies of cSVD remain inconclusive. The aim of this systematic review and meta‐analysis was to characterize the associations between cSVD and cerebrovascular reactivity (CVR), cerebral autoregulation, and arterial stiffness (AS). Methods and Results: MEDLINE, Web of Science, and Embase were searched from inception to September 2023 for studies reporting CVR, cerebral autoregulation, or AS in relation to radiological markers of cSVD. Data were extracted in predefined tables, reviewed, and meta‐analyses performed using inverse‐variance random effects models to determine pooled odds ratios (ORs). A total of 1611 studies were identified; 142 were included in the systematic review, of which 60 had data available for meta‐analyses. Systematic review revealed that CVR, cerebral autoregulation, and AS were consistently associated with cSVD (80.4%, 78.6%, and 85.4% of studies, respectively). Meta‐analysis in 7 studies (536 participants, 32.9% women) revealed a borderline association between impaired CVR and cSVD (OR, 2.26 [95% CI, 0.99–5.14]; P =0.05). In 37 studies (27 952 participants, 53.0% women) increased AS, per SD, was associated with cSVD (OR, 1.24 [95% CI, 1.15–1.33]; P <0.01). Meta‐regression adjusted for comorbidities accounted for one‐third of the AS model variance ( R ² =29.4%, P _moderators =0.02). Subgroup analysis of AS studies demonstrated an association with white matter hyperintensities (OR, 1.42 [95% CI, 1.18–1.70]; P <0.01). Conclusions: The collective findings of the present systematic review and meta‐analyses suggest an association between cSVD and impaired CVR and elevated AS. However, longitudinal investigations into vascular stiffness and regulatory function as possible risk factors for cSVD remain warranted.

5-fluorouracil (5-FU) is the second most common cancer chemotherapy associated with short- and long-term cardiotoxicity. Although the mechanisms mediating these toxicities are not well understood, patients often present with symptoms suggestive of microvascular dysfunction. We tested the hypotheses that patients undergoing cancer treatment with 5-FU based chemotherapy regimens would present with impaired microvascular reactivity and that these findings would be substantiated by decrements in endothelial nitric oxide synthase (eNOS) gene expression in 5-FU treated human coronary artery endothelial cells (HCAEC). We first performed a cross-sectional analysis of 30 patients undergoing 5-FU based chemotherapy treatment for cancer (5-FU) and 32 controls (CON) matched for age, sex, body mass index, and prior health history (excluding cancer). Cutaneous microvascular reactivity was evaluated by laser Doppler flowmetry in response to endothelium-dependent (local skin heating; acetylcholine iontophoresis, ACh) and -independent (sodium nitroprusside iontophoresis, SNP) stimuli. In vitro experiments in HCAEC were completed to assess the effects of 5-FU on eNOS gene expression. 5-FU presented with diminished microvascular reactivity following eNOS-dependent local heating compared to CON (P = 0.001). Iontophoresis of the eNOS inhibitor L-NAME failed to alter the heating response in 5-FU (P = 0.95), despite significant reductions in CON (P = 0.03). These findings were corroborated by lower eNOS gene expression in 5-FU treated HCAEC (P < 0.01) compared to control. Peak vasodilation to ACh (P = 0.58) nor SNP (P = 0.39) were different between groups. The present findings suggest diminished microvascular function along the eNOS-NO vasodilatory pathway in patients with cancer undergoing treatment with 5-FU-based chemotherapy regimens and thus, may provide insight into the underlying mechanisms of 5-FU cardiotoxicity.

Cancer survivors are at greater risk for cardiovascular disease (CVD) than second malignancy, resulting in a decreased quality of life and increased cost of care. Additional knowledge of CVD prevention by identifying possible risk factors has clinical relevance. Our main objective was to determine the relevance of a clinical index of arterial stiffness, pulse pressure, in predicting CVD mortality in cancer patients, with a second objective to examine its relationship with cancer mortality. We retrospectively analyzed 781 cancer patients from Third National Health and Nutrition Examination Survey and Linked Mortality File, including demographic, anthropometric, blood pressure, and cause of death. Kaplan-Meier survival curve and Cox hazard regression analyses were performed to assess the relationship between pulse pressure and cardiovascular, cancer, and all-cause mortality. During a mean follow-up time of 8.1 years, 603 deaths, 257 cancer and 151 CVD, occurred. In unadjusted models, the risk of CVD, cancer, and all-cause mortality were 3.8-fold, 5.3-fold, and 1.6-fold higher, respectively, for pulse pressure ≥70 ​mmHg compared to <50 ​mmHg. Adjusted analyses revealed a higher CVD mortality in cancer patients <65 years with a pulse pressure 60–70 ​mmHg (adjusted hazard ratio, 5.26; 95%CI, 1.12–24.78) when compared to pulse pressure of <50 ​mmHg. Pulse pressure was not associated with risk of all-cause, CVD, or cancer in those ≥65 years. Pulse pressure, an index of arterial stiffness, is predictive of CVD mortality in cancer patients. Our findings support non-invasive office-setting measurements of arterial stiffness to identify high risk patients.

Purpose: Cancer patients with a history of radiotherapy are at an increased risk of ischemic heart disease. Preclinical animal studies demonstrate markedly impaired acetylcholine (ACh)-mediated endothelium-dependent vasorelaxation within days to weeks post-irradiation, however, whether microvascular function is affected in the intact human circulation during cancer radiation therapy has yet to be determined. Materials and methods: Using laser-Doppler flowmetry, microvascular endothelium-dependent and independent responses were evaluated through iontophoresis of acetylcholine (ACh) (part 1, n = 7) and sodium nitroprusside (SNP) (part 2, n = 8), respectively, in women currently receiving unilateral chest adjuvant radiation therapy for breast cancer. Measurements were performed at the site of radiation treatment and at a contralateral control, non-radiated site. Cutaneous vascular conductance (CVC) was calculated by normalizing for mean arterial pressure. Results and Conculsions: In part 1, patients received an average radiation dose of 2104 ± 236 cGy. A significantly lower peak ACh-mediated endothelium-dependent vasodilation was observed within the radiated microvasculature when compared to non-radiated (radiated: 532 ± 167%, non-radiated 1029 ± 263%; P = 0.02). In part 2, the average radiation dose received was 2251 ± 196 cGy. Iontophoresis of SNP elicited a similar peak endothelium-independent vasodilator response in radiated and non-radiated tissue (radiated: 179 ± 58%, non-radiated: 310 ± 158; P = 0.2). The time to 50% of the peak response for ACh and SNP was similar between radiated and non-radiated microvasculature (P < 0.05). These data provide evidence of early endothelium-dependent microvascular dysfunction in cancer patients currently receiving chest radiation and provide the scientific premise for future work evaluating coronary endothelial function and vasomotor reactivity using more detailed and invasive procedures.

Athletes are susceptible to acute respiratory tract infections, including SARS-CoV-2, which can affect cardiovascular function. We aimed to evaluate the impact of COVID-19 infection and quarantine on cardiac function in male and female collegiate athletes. We conducted a single-center, prospective, case-control study and performed transthoracic echocardiography in a diverse group of convalescent SARS-CoV-2-positive athletes following a 10-14-day quarantine, matched to non-SARS-CoV-2 athletes. Data collection occurred from August 1, 2020, to May 31, 2021. We evaluated 61 SARS-CoV-2-positive athletes (20 ± 1 years, 39% female) and 61 controls (age 20 ± 2 years, 39% female). Echocardiography in SARS-CoV-2-positive athletes was performed on average 40 ± 38 days after infection diagnosis. All SARS-CoV-2-positive athletes had clinically normal systolic left ventricular function (LVEF > 50%). However, SARS-CoV-2-positive athletes exhibited mildly lower LVEF compared to controls (65 ± 6% vs. 72 ± 8%, respectively, p < 0.001), which remained significant when evaluated separately for female and male athletes. Sub-analysis revealed these differences occurred only when imaging occurred within a mean average of 27 days of infection, with a longer recovery period (≥27 days) resulting in no differences. SARS-CoV-2-positive male athletes exhibited higher left ventricular end-diastolic volume and mitral filling velocities compared to male controls. Our study reveals unique sex-specific cardiac changes in collegiate athletes following SARS-CoV-2 infection and quarantine compared to controls. Despite a mild reduction in LVEF, which was only observed in the first weeks following infection, no clinically significant cardiac abnormalities were observed. Further research is required to understand if the changes in LVEF are directly attributed to the infection or indirectly through exercise restrictions resulting from quarantine.