Arterial structure and function change progressively with advancing age. Owing to long-lasting repetitive stretch with intermittent cardiac contraction, elastic fibers in the tunica media of large arteries gradually degenerate and are replaced by collagenous fibers. Such medial degeneration causes elastic arteries to stiffen and dilate. However, the speed of the vascular aging varies considerably among individuals; a discrepancy often exists between the chronological age of an individual and the biological age of his or her arteries. In susceptible individuals the vascular aging process can be accelerated under the presence of various risk factors including hypertension, smoking, metabolic disorders, high sodium intake and hereditary traits. Early vascular aging is generally detected by vascular function tests such as pulse wave velocity (PWV) and pulse wave analysis. Stiffening of large elastic arteries increases the PWV, increases the amplitude of the incident pressure wave, and hastens the return of the reflected pressure wave. Consequent widening of the aortic pulse pressure elevates left ventricular afterload during systole and reduces coronary flow during diastole, thus predisposing to heart failure and myocardial ischemia. The excessive pulsatile pressure is also transmitted into the vulnerable microvasculature in the kidney and brain to cause albuminuria and lacunar infarction. Furthermore, aortic stiffening increases blood flow reversal in early diastole in the proximal descending aorta. The increased aortic flow reversal reduces renal blood flow and glomerular filtration rate, and in addition, it raises the risk of retrograde cerebral embolism of aortic mobile plaques. Such deleterious impacts of the central hemodynamic abnormalities on the vital end-organs predispose the patients with early vascular aging to premature cardiovascular diseases. Indeed, epidemiological prospective studies have demonstrated that aortic PWV and central hemodynamic indices predict the occurrence of cardiovascular diseases including myocardial infarction, stroke and end-stage renal disease. Although vascular aging is considered an inevitable and irreversible process, it can be delayed through lifestyle modification and/or de-stiffening therapy with effective antihypertensive medication. Therefore, early prevention of vascular aging is a key strategy to reduce cardiovascular risk and improve prognosis in patients with hypertension.
Recent research has noted a pathological link between the heart and kidney, known as cardio-renal syndrome. However, little is clear about the pathophysiological mechanism behind it. A relationship of altered central hemodynamics to microalbuminuria in hypertension has been demonstrated ( Hypertension 2011;58:839-846). The present study was conducted to investigate two hypotheses: 1) a link between albuminuria and plasma B-type natriuretic peptide (BNP); and 2) involvement of central hemodynamics in this link. In 392 patients with uncomplicated hypertension (age, 56±12 years), the radial pressure waveforms were recorded with applanation tonometry to estimate the central aortic pressure parameters. The pulse wave velocity (PWV) was measured in carotid-femoral (aortic) and carotid-radial (peripheral) regions. Albuminuria was defined as urinary albumin/creatinine ratio (UACR) ≥30 mg/g of creatinine. The log-transformed BNP (median, 14 pg/ml) was correlated ( P ≤0.006) with aortic systolic ( r =0.31) and pulse ( r =0.46) pressures, aortic forward ( r =0.41) and augmented ( r =0.26) pressures, mean arterial pressure ( r =0.14), and aortic ( r =0.39) but not peripheral ( r =–0.09) PWV. The correlation with the aortic pulse pressure tended to be closer than the brachial pulse pressure ( P =0.07). The BNP was correlated ( P <0.001) positively with UACR ( r =0.34), and negatively with estimated glomerular filtration rate (eGFR, r =–0.39). The presence of albuminuria was associated with an elevation of BNP (≥40 pg/ml) in a stepwise logistic model adjusted for age, body mass index, diabetes, eGFR, use of renin-angiotensin inhibitors and β-blockers (odds ratio: 2.74; P =0.007). Of note, however, additional adjustment for the aortic pulse pressure rendered this association statistically insignificant, and the aortic pulse pressure emerged as the strongest predictor of the BNP elevation (odds ratio: 1.41 per 10mmHg increase; P =0.003). In each patient subgroup with normo-, micro-, and macro-albuminuria, wider aortic pulse pressure was always associated with higher BNP level. In conclusion, albuminuria and elevated BNP are closely connected in hypertension. The central hemodynamics plays a pivotal role in mediating this cardio-renal connection.
Miyagi University of Education Medical Center, Sendai, Japan Correspondence to Junichiro Hashimoto, MD, PhD, Medical Center, Miyagi University of Education, 149 Aoba, Aramaki, Aoba-ku, Sendai, Miyagi 980-0845, Japan. E-mail: [email protected]
The authors have developed an uncollimated sheet line source with a fluoroplastic tube for gamma ray transmission CT (TCT). This source filled with Tc-99m was attached to the collimator face on one head of a dual head single photon emission computed tomography (SPECT) system. In simultaneous SPECT/TCT scans using Tl-201 as the SPECT source and Tc-99m as the TCT source, scatter and spilldown contamination in the Tc-99m (141 keV) data and the Tl-201 (75 keV) data can be removed with the triple energy window (TEW) method. However, lead X-ray contamination in the Tl-201 data cannot be removed with the TEW method. The authors have developed an estimation method of the lead X-ray contamination in the Tl-201 data. This method depends on the hypothesis that the lead X-ray is proportional to the amount of attenuating media and primary photons along each projection path. The amount of attenuating media is given by a transmission image and that of primary photons is estimated by the TEW method. The coefficients needed for this estimation are experimentally determined by only Tc-99m TCT scan data The feasibility of the proposed method was demonstrated by a chest phantom study and a myocardial clinical study.
We evaluated the safety and clinical usefulness of the same day protocol of exercise 99mTc-MIBI SPECT in 107 patients with heart diseases. No adverse event was observed except for one case of transient hypotension caused by the exercise. More than 95% of stress images and all of the rest images were judged as "Excellent" or "Good" in image quality. Overall sensitivity was 84.3% in detecting coronary artery disease, and no statistical difference was observed between the results obtained with Re-Ex and Ex-Re protocols. The examination was "Quite Effective" or "Effective" in diagnostic efficacy in 96.2% of the cases. We concluded that the same day protocol is a safe and useful method for diagnosing myocardial ischemia, which provides high image quality and valuable information.
Background and Purpose— Ambulatory arterial stiffness index (AASI) and pulse pressure (PP) are indexes of arterial stiffness and can be computed from 24-hour blood pressure recordings. We investigated the prognostic value of AASI and PP in relation to fatal outcomes. Methods— In 1542 Ohasama residents (baseline age, 40 to 93 years; 63.4% women), we applied Cox regression to relate mortality to AASI and PP while adjusting for sex, age, BMI, 24-hour MAP, smoking and drinking habits, diabetes mellitus, and a history of cardiovascular disease. Results— During 13.3 years (median), 126 cardiovascular and 63 stroke deaths occurred. The sex- and age-standardized incidence rates of cardiovascular and stroke mortality across quartiles were U-shaped for AASI and J-shaped for PP. Across quartiles, the multivariate-adjusted hazard ratios for cardiovascular and stroke death significantly deviated from those in the whole population in a U-shaped fashion for AASI, whereas for PP, none of the HRs departed from the overall risk. The hazard ratios for cardiovascular mortality across ascending AASI quartiles were 1.40 ( P =0.04), 0.82 ( P =0.25), 0.64 ( P =0.01), and 1.35 ( P =0.03). Additional adjustment of AASI for PP and sensitivity analyses by sex, excluding patients on antihypertensive treatment or with a history of cardiovascular disease, or censoring deaths occurring within 2 years of enrollment, produced confirmatory results. Conclusions— In a Japanese population, AASI predicted cardiovascular and stroke mortality over and beyond PP and other risk factors, whereas in adjusted analyses, PP did not carry any prognostic information.
Abstract BACKGROUND Central pulse pressure (cPP) is responsible for the hemodynamics of vital organs, and monitoring this parameter is important for cardiovascular disease (CVD) prevention. Excess sodium intake and (micro)albuminuria (a manifestation of renal microvascular damage) are known to be strong predictors of CVD. We sought to investigate the cross-sectional relationships among dietary sodium intake, albuminuria, and cPP in a general population cohort. METHODS The subjects were 933 apparently healthy adults (mean age, 56 ± 10 years). Radial pressure waveforms were recorded with applanation tonometry to estimate mean arterial pressure (MAP), cPP, forward and backward pressure amplitudes, and augmentation index. The urinary sodium/creatinine and albumin/creatinine ratios were measured in spot urine samples. RESULTS Both the urinary sodium/creatinine and albumin/creatinine ratios were positively correlated with cPP, even after adjusting for MAP (P < 0.001). Moreover, both ratios had a synergistic influence on increasing the cPP independent of age, sex, estimated glomerular filtration rate, hyperlipidemia, and diabetes (interaction P = 0.04). A similar synergistic influence was found on the forward pressure amplitude, but not on the backward pressure amplitude or augmentation index. The overall results were not altered when the urinary albumin/creatinine ratio was replaced with the existence of chronic kidney disease (CKD). CONCLUSIONS (Micro)albuminuria strengthens the positive association between urinary sodium excretion and cPP and systolic forward pressure. Excess sodium intake may magnify the cardiovascular risk by widening the aortic pulsatile pressure, particularly in the presence of concomitant CKD.
There is continuing controversy over whether the pattern of circadian blood pressure (BP) variation that includes a nocturnal decline in BP and a morning pressor surge has prognostic significance for stroke risk. In this study, we followed the incidence of stroke in 1430 subjects aged ≥40 years in Ohasama, Japan, for an average of 10.4 years. The association between stroke risk and the pattern of circadian BP variation was analyzed with a Cox proportional hazards model after adjustment for possible confounding factors. There was no significant association between total stroke risk and the nocturnal decline in BP (percentage decline from diurnal level) or between total stroke risk and the morning pressor surge. The cerebral infarction risk was significantly higher in subjects with a <10% nocturnal decline in BP as compared with subjects who had a ≥10% nocturnal decline in BP ( P =0.04). The morning pressor surge was not associated with a risk of cerebral infarction. On the other hand, an increased risk of cerebral hemorrhage was observed in subjects with a large morning pressor surge (≥25 mm Hg; P =0.04). Intracerebral hemorrhage was also observed more frequently in extreme dippers (those with a ≥20% nocturnal decline in BP) than dippers (those with a 10% to 19% decline; P =0.02). A disturbed nocturnal decline in BP is associated with cerebral infarction, whereas a large morning pressor surge and a large nocturnal decline in BP, which are analogous to a large diurnal increase in BP, are both associated with cerebral hemorrhage.
