Heart rate variability (HRV) represents one of the most promising markers of the autonomic nervous system (ANS) regulation. However, it requires the acquisition of the ECG signal in order to reliably detect the RR intervals, which is not always easily and comfortably available in personal health applications. Additionally, due to progress in single spot optical sensors, photoplethysmography (PPG) is an interesting alternative for heartbeat interval measurements, since it is a more convenient and a less intrusive measurement technique. Driven by the technological advances in such sensors, wrist-worn devices are becoming a commodity, and the interest in the assessment of HRV indexes from the PPG analysis (pulse rate variability - PRV) is rising. In this study, we investigate the hypothesis of using PRV features as surrogates for HRV indexes, in three different contexts: healthy subjects at rest, healthy subjects after physical exercise and subjects with cardiovascular diseases (CVD). Additionally, we also evaluate which are the characteristic points better suited for PRV analysis in these contexts, i.e. the PPG waveform characteristic points leading to the PRV features that present the best estimates of HRV (correlation and error analysis). The achieved results suggest that the PRV can be often used as an alternative for HRV analysis in healthy subjects, with significant correlations above 82%, for both time and frequency features. Contrarily, in the post-exercise and CVD subjects, time and (most importantly) frequency domain features shall be used with caution (mean correlations ranging from 68% to 88%).

AMPK activation during ischemia helps the myocardium to cope with the deficit of energy production. As AMPK activity is considered to be impaired in diabetes, we hypothesized that enhancing AMPK activation during ischemia above physiological levels would protect the ischemic diabetic heart through AMPK activation and subsequent inhibition of mitochondrial permeability transition pore (mPTP) opening. Isolated perfused hearts from normoglycemic Wistar or diabetic Goto-Kakizaki (GK) rats (n ≥ 6/group) were subjected to 35 min of ischemia in the presence of 10, 20, and 40 μM of A-769662, a known activator of AMPK, followed by 120 min of reperfusion with normal buffer. Myocardial infarction and AMPK phosphorylation were assessed. The effect of A-769662 on mPTP opening in adult cardiomyocytes isolated from both strains was also determined. A-769662 at 20 μM reduced infarct size in both Wistar (30.5 ± 2.7 vs. 51.8 ± 3.9% vehicle; P < 0.001) and GK hearts (22.7 ± 3.0 vs. 48.5 ± 4.7% vehicle; P < 0.001). This protection was accompanied by a significant increase in AMPK and GSK-3β phosphorylation. In addition, A-769662 significantly inhibited mPTP opening in both Wistar and GK cardiomyocytes subjected to oxidative stress. We demonstrate that AMPK activation during ischemia via A-769662 reduces myocardial infarct size in both the nondiabetic and diabetic rat heart. Furthermore, this cardioprotective effect appears to be mediated through inhibition of mPTP opening. Our findings suggest that improving AMPK activation during ischemia can be another mechanism for protecting the ischemic heart.

In recent years, the role of arterial stiffness in the development of cardiovascular diseases has been explored more extensively. Local arterial stiffness may be gauged via ultrasound, measuring pulse transit time relative to changing vessel diameters and distending pressures. Recently, direct vessel-wall tracking systems have been devised based on new ultrasonographic methodologies, such as tissue Doppler imaging and speckle-tracking analysis—vascular mechanics. These advances have been evaluated in varying arterial distributions, are proved surrogates of pulse wave velocity, and are ascending in clinical importance. In the course of this review, we describe fundamental concepts and methodologies involved in ultrasound assessment of vascular mechanics. We also present relevant clinical studies and discuss the potential clinical utility of such diagnostic pursuits.

Some patients show such an important clinical improvement and reverse remodelling after cardiac resynchronization therapy (CRT) that anatomy and function approach normal. These patients have been called ‘super-responders’. The aim of our study was to identify predictors of becoming a super-responder after CRT. Eighty-seven consecutive patients who underwent CRT were prospectively studied. Before CRT and 6 months after, clinical and echocardiographic evaluation was performed. Patients with a decrease in New York Heart Association functional class ≥1, a two-fold or more increase of left ventricular ejection fraction (LVEF) or a final LVEF >45%, and a decrease in LV end-systolic volume >15% were classified as super-responders. There were 12% super-responders. At baseline, there were no significant differences between super-responders and the other patients, except for the fact that super-responders had significantly smaller mitral regurgitation and LV end-diastolic diameter (LVEDD) and a shorter duration of heart failure symptoms. Mitral regurgitation jet area, LVEDD, and duration of heart failure symptoms were correlated with this super-response. Moreover, an evolution of symptoms for <12 months was an independent predictor of super-response to CRT. Patients in earlier phases of the cardiomyopathy, with a less altered ventricular geometry, seem to have a greater probability of becoming super-responders.