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Aims : Patients with mild heart failure (HF) who are clinically compensated may have normal left ventricular (LV) stroke volume (SV). Despite this, altered intra-ventricular flow patterns have been recognized in these subjects. We hypothesized that, compared with normal LVs, flow in myopathic LVs would demonstrate a smaller proportion of inflow volume passing directly to ejection and diminished the end-diastolic preservation of the inflow kinetic energy (KE). Methods and results : In 10 patients with dilated cardiomyopathy (DCM) (49 ± 14 years, six females) and 10 healthy subjects (44 ± 17 years, four females), four-dimensional MRI velocity and morphological data were acquired. A previously validated method was used to separate the LV end-diastolic volume (EDV) into four flow components based on the blood's locations at the beginning and end of the cardiac cycle. KE was calculated over the cardiac cycle for each component. The EDV was larger (P = 0.021) and the ejection fraction smaller (P < 0.001) in DCM compared with healthy subjects; the SV was equivalent (DCM: 77 ± 19, healthy: 79 ± 16 mL). The proportion of the total LV inflow that passed directly to ejection was smaller in DCM (P = 0.000), but the end-diastolic KE/mL of the direct flow was not different in the two groups (NS). Conclusion : Despite equivalent LVSVs, HF patients with mild LV remodelling demonstrate altered diastolic flow routes through the LV and impaired preservation of inflow KE at pre-systole compared with healthy subjects. These unique flow-specific changes in the flow route and energetics are detectable despite clinical compensation, and may prove useful as subclinical markers of LV dysfunction.

Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 5 uppsatser.

A research report submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in partial fulfillment of the requirements for the degree of Master of Medicine. Johannesburg, October 2017. / Background: Positron Emission Tomography (PET) is an imaging modality that guides the revascularization management of patients with left ventricular systolic dysfunction secondary to coronary artery disease. Segments of the myocardium demonstrating reduced perfusion and increased or preserved 18FFluorodeoxyglucose (18F-FDG) uptake are considered to be viable and thus suitable for revascularization. The aim of our study was to determine the prevalence of myocardial viability as determined by FDG-PET in our local cohort and to compare our prevalence of myocardial viability to data published elsewhere. Methods: We retrospectively reviewed 240 consecutive 99mTc-sestamibi myocardial perfusion Gated Single Photon Emission Tomography (SPECT) and 18FFDG PET reports of patients referred for evaluation of myocardial viability between January 2009 and June 2015. Results: 236 patients met the inclusion criteria. There were 194 (82.2%) males. The mean age was 59.1 (SD 11.0) years. A total of 4012 segments of the left ventricle were analyzed on the gated SPECT and reduced perfusion was noted in 1862 (46.4%) segments. Perfusion-metabolism mismatch (viable myocardium) was observed in 586 (31.5%) out of 1862 perfusion defects. The prevalence of myocardial viability in the study population was 61.4%. On the multivariate logistic regression model, aspirin intake [OR:0.37; CI:0.16-0.83; p=0.016] and hypertension [OR:0.26; CI:0.12-0.58; p=0.001] were associated with the presence of viable myocardium. Smoking was associated with the likelihood of having non-viable myocardium [OR:2.31; CI:1.01-5.29; p=0.048] Conclusion: The prevalence of myocardial viability as detected by 18F FDG PET in our local cohort is similar to prevalence rates reported in the developed world. / LG2018

In this thesis, we included results from two studies. The first one considered the effects of the blood volume changes, during blood donation, on the heart rate variability (HRV) measured, non-invasively, form electrocardiographic (ECG) and photoplethysmographic (PPG) signals. Our results showed that, during blood donation, there were no significant changes in the pulsatile area of PPG signal, while heart rate increased. No significant changes were noticed in HRV extracted from both signals. Error analysis between the HRV extracted from ECG and peak interval variability (PIV) suggested that the error during blood donation was increased which means that the use of PIV extracted from PPG signal, used as a replacement diagnostic tool in clinical applications, needs further investigations and should be carefully studied in non-stationary cardiovascular situations such as blood donation. The imbalance between the two branches of the autonomic nervous system, sympathetic and parasympathetic, vagal, may result in a harmful activation of myocardial tissues which cause arrhythmias and sudden cardiac death. Although the study of the sympathovagal balance have been attracting many researchers, further studies are needed to elucidate the effects of many kinds of drugs on the autonomic modulation of the cardiac muscle, specifically, the cells of sinoatrial (SA) node. The aim of the second part of this thesis was to assess the effects of calcium channel blocker (Verapamil), calcium channel sensitizer (Levosimendan), calcium chloride (CaCl2), the combinations of verapamil/ CaCl2, levosimendan/ CaCl2, and noradrenaline infusion on beat-to-beat cardiovascular variability represented, in this research, by systolic blood pressure variability (SBPV), and stroke volume variability (SVV) signals. We used Fat Fourier Transform (FFT) to evaluate the power spectral density of the fluctuations in both signals to evaluate the effects of short-term treatments with those drugs on the sympathovagal balance in normal rats. Then, we compared the spectra obtained from SBPV and SVV to decide which of these fluctuations along with corresponding spectrum was more able to provide a clear feedback about the autonomic nervous system. Our data suggests that there were a significant correlations between low- (LF), mid- (MF), and high-frequency (HF) spectra obtained from SBPV and SVV except between the HF spectra estimated from after the infusion of levosimendan where a poor correlation (r = 0.530, p = 0.281) was noticed. This that both HF components obtained provide different information regarding the autonomic nervous system modulation of the SA node cells, while the results obtained from the rest of experiments showed that both signals provide same information about the modulation of sympathetic and parasympathetic tone due to all stages of different drugs infusion studied in this thesis. Besides that, we found that both spectra may be used to track the fluctuations in the cardiac output as a result of the drugs infusion.

In this thesis, we included results from two studies. The first one considered the effects of the blood volume changes, during blood donation, on the heart rate variability (HRV) measured, non-invasively, form electrocardiographic (ECG) and photoplethysmographic (PPG) signals. Our results showed that, during blood donation, there were no significant changes in the pulsatile area of PPG signal, while heart rate increased. No significant changes were noticed in HRV extracted from both signals. Error analysis between the HRV extracted from ECG and peak interval variability (PIV) suggested that the error during blood donation was increased which means that the use of PIV extracted from PPG signal, used as a replacement diagnostic tool in clinical applications, needs further investigations and should be carefully studied in non-stationary cardiovascular situations such as blood donation. The imbalance between the two branches of the autonomic nervous system, sympathetic and parasympathetic, vagal, may result in a harmful activation of myocardial tissues which cause arrhythmias and sudden cardiac death. Although the study of the sympathovagal balance have been attracting many researchers, further studies are needed to elucidate the effects of many kinds of drugs on the autonomic modulation of the cardiac muscle, specifically, the cells of sinoatrial (SA) node. The aim of the second part of this thesis was to assess the effects of calcium channel blocker (Verapamil), calcium channel sensitizer (Levosimendan), calcium chloride (CaCl2), the combinations of verapamil/ CaCl2, levosimendan/ CaCl2, and noradrenaline infusion on beat-to-beat cardiovascular variability represented, in this research, by systolic blood pressure variability (SBPV), and stroke volume variability (SVV) signals. We used Fat Fourier Transform (FFT) to evaluate the power spectral density of the fluctuations in both signals to evaluate the effects of short-term treatments with those drugs on the sympathovagal balance in normal rats. Then, we compared the spectra obtained from SBPV and SVV to decide which of these fluctuations along with corresponding spectrum was more able to provide a clear feedback about the autonomic nervous system. Our data suggests that there were a significant correlations between low- (LF), mid- (MF), and high-frequency (HF) spectra obtained from SBPV and SVV except between the HF spectra estimated from after the infusion of levosimendan where a poor correlation (r = 0.530, p = 0.281) was noticed. This that both HF components obtained provide different information regarding the autonomic nervous system modulation of the SA node cells, while the results obtained from the rest of experiments showed that both signals provide same information about the modulation of sympathetic and parasympathetic tone due to all stages of different drugs infusion studied in this thesis. Besides that, we found that both spectra may be used to track the fluctuations in the cardiac output as a result of the drugs infusion.

These studies determined the effects of sodium chloride supplementation on serum and sweat sodium concentration, cardiovascular function, and physical and cognitive performance. Sweat sodium losses, alone, caused a significant decline in serum sodium concentration (-6.4±1.6 mEq/L, p=0.001) during 3h cycling in the heat in endurance-trained athletes with high sweat sodium losses. However, sodium chloride supplementation matching sweat sodium losses (NA; 5.9±1.5g NaCl/h) maintained serum sodium concentration. Post-exercise maximal cycling power declined and was significantly lower than pre-exercise in placebo (PL; p=0.012), but power was not significantly different in NA (p=0.057). Pre- to post-exercise response time during a Stroop Test improved in NA (p=0.009), while there was no change in PL (p=0.597). Post-exercise postural sway was less in NA vs. PL (p=0.044). Three days of sodium chloride supplementation (~15 g NaCl/d) resulted in a significant increase in plasma volume in healthy untrained males at rest (5.9±7.6 %) and during exercise at 60%VO₂peak (8.6±5.2 %) compared to PL. During NA, stroke volume was 10% higher during exercise vs. PL (139±27 vs. 126±24 ml/beat, respectively, p=0.004). Cardiac output was 8% higher in NA during exercise vs. PL (21.0±3.1 vs. 19.4±2.6 L/min, respectively, p=0.013). Mean arterial pressure during exercise was not different in NA vs. PL (p=0.548) as total peripheral resistance decreased (p=0.027) with the increased cardiac output. Sweat sodium concentration was 9% higher in NA vs. PL during exercise in the heat (70.4±19.5 vs. 64.5±21.7 mEq/L, p=0.044). In summary, serum sodium concentration declines when high sweat sodium losses are not replaced while hydration status is maintained. Acute sodium chloride supplementation during exercise which matches sodium losses maintains serum sodium concentration. This maintenance of serum sodium concentration results in both physical and cognitive benefits compared to when serum sodium concentration declines. Chronic intake of sodium chloride for 3 days increases plasma volume in healthy untrained men and improves cardiovascular function, as both stroke volume and cardiac output are increased, while oxygen consumption and blood pressure are unchanged. Therefore, acute and chronic sodium supplementation positively alters fluid and sodium balance which results in beneficial effects on physical and cognitive performance and cardiovascular function during exercise. / text

Slow and deep breathing (SDB) has long been regarded as a nonpharmacological method for dealing with several physiological and emotional imbalances, and widely used for relaxation purposes. There is, however, limited understanding of the putative mechanisms by which SDB acutely impacts the cardiovascular and autonomic systems to elicit chronic adaptations. The present thesis explored how the manipulation of breathing pattern and intrathoracic pressure during SDB could further the understanding of the regulatory mechanisms that underpin the acute cardiovascular response to SDB. This thesis makes an original contribution to the existing knowledge by reporting a previously undescribed inversion of normal within-breath (inspiration vs. expiration) left ventricular stroke volume (LVSV) pattern for breathing frequencies < 8 breaths∙min-1. This finding might reflect the influence of a lag between enhanced right atrial filling and right ventricular stroke volume during inspiration, and its expression in left ventricular stroke volume; this lag results from the time required for blood to transit the pulmonary circulation. Furthermore, blood pressure variability (BPV) was reduced significantly at the lowest breathing frequencies, likely due to the involvement of baroreflex mediated responses. The pattern of responses was consistent with the buffering of respiratory-driven fluctuations in left ventricular cardiac output (Q̇) and arterial blood pressure (ABP) by within breath fluctuations in heart rate (fc), i.e., respiratory sinus arrhythmia (RSA) (Chapter 4). Chapter 5 demonstrated that magnifying negative intrathoracic pressure with inspiratory loading during SDB increased inspiratory pressure-driven fluctuations in LVSV and fc, and enhanced Q̇, independently of changes in VT and fR. The data support an important contribution to the amplification of RSA, during SDB, of previously underappreciated reflex, and/or 'myogenic', cardiac response mechanisms. The findings in Chapter 6 confirmed that inspiratory loading during SDB amplified the effects observed with un-loaded SDB (reported in chapter 5). In contrast, expiratory loading increased ABP and attenuated RSA, LVSV and Q̇ during SDB. A lower RSA for higher ABP, supports the presence of a formerly underappreciated contribution of sinoatrial node stretch to RSA, and throws into question the clinical benefits of expiratory resisted SDB, particularly in hypertensive populations. In conclusion, the findings of the present thesis provide novel information regarding the mechanisms contributing to acute cardiovascular response to SDB. These new insights may contribute to the development of more effective SDB interventions, geared towards maximising the perturbation to the cardiovascular control systems.

<p>Large quantities of data have described left ventricular adaptation to endurance training, but basic concepts on left ventricular performance during exercise remain controversial. In this thesis, we present the results of studies of left ventricular dynamics during exercise in 89 endurance-trained athletes.</p><p>Using radionuclide ventriculography, 35 female and 30 male endurance athletes were studied in supine position. During supine exercise at 70% of the age-expected maximal heart rate, the adjustments in left ventricular volumes were small, suggesting a high preload before exercise. Stroke volume increased by changes in the left ventricular end-diastolic volumes but no changes were observed in the end-systolic volumes. Moreover, no significant differences were noted between male and female athletes.</p><p>Contrast echocardiography was utilized when 24 male endurance athletes were studied during upright exercise. An almost linear increase in stroke volume was seen from upright rest to upright exercise at a heart rate of 160 beats per minute. Stroke volume increased by an almost linear increase in end-diastolic volume and showed an initial small decrease in end-systolic volume. The left ventricular cavity became geometrically more spherical with the largest increase in the left ventricular end-diastolic short-axis cavity diameters in the mid and apical part of the left ventricle. Left ventricular long-axis length obtained from the epicardial apex to the middle of the mitral annulus at end-diastole showed no significant change from rest to exercise. The mitral annulus motion contributed to more than 50% of the stroke volume during exercise with no significant difference between septal and lateral annular motion at peak exercise. Major changes were observed in left ventricular filling indices during upright exercise. The mean transmitral pressure gradient showed a linear increase and increased several times as the mean diastolic time decreased, with large reductions in mean left ventricular filling time. Despite the shortened filling time, the heart was able to increase the filling rate (measured as volume per time) five times. This observation verifies that the heart has large reserves at rest and reveals the increase in capacity during exercise.</p>

Large quantities of data have described left ventricular adaptation to endurance training, but basic concepts on left ventricular performance during exercise remain controversial. In this thesis, we present the results of studies of left ventricular dynamics during exercise in 89 endurance-trained athletes. Using radionuclide ventriculography, 35 female and 30 male endurance athletes were studied in supine position. During supine exercise at 70% of the age-expected maximal heart rate, the adjustments in left ventricular volumes were small, suggesting a high preload before exercise. Stroke volume increased by changes in the left ventricular end-diastolic volumes but no changes were observed in the end-systolic volumes. Moreover, no significant differences were noted between male and female athletes. Contrast echocardiography was utilized when 24 male endurance athletes were studied during upright exercise. An almost linear increase in stroke volume was seen from upright rest to upright exercise at a heart rate of 160 beats per minute. Stroke volume increased by an almost linear increase in end-diastolic volume and showed an initial small decrease in end-systolic volume. The left ventricular cavity became geometrically more spherical with the largest increase in the left ventricular end-diastolic short-axis cavity diameters in the mid and apical part of the left ventricle. Left ventricular long-axis length obtained from the epicardial apex to the middle of the mitral annulus at end-diastole showed no significant change from rest to exercise. The mitral annulus motion contributed to more than 50% of the stroke volume during exercise with no significant difference between septal and lateral annular motion at peak exercise. Major changes were observed in left ventricular filling indices during upright exercise. The mean transmitral pressure gradient showed a linear increase and increased several times as the mean diastolic time decreased, with large reductions in mean left ventricular filling time. Despite the shortened filling time, the heart was able to increase the filling rate (measured as volume per time) five times. This observation verifies that the heart has large reserves at rest and reveals the increase in capacity during exercise.