BACKGROUND AND OBJECTIVES: Smoking increases cardiovascular risk and it is known to acutely increase arterial stiffness in healthy smokers. We investigated the acute and chronic effects of smoking on the arterial mechanics in smokers with hypertension. SUBJECTS AND METHODS: To evaluate the acute effects of smoking, the heart rate (HR), brachial blood pressure (BP), ankle systolic BP, heart-carotid pulse wave velocity (hcPWV), heart-femoral PWV (hfPWV), femoral-ankle PWV (faPWV), heart-brachial PWV (hbPWV), and the ankle-brachial index (ABI) were measured in male hypertensive smokers (n=22, 42+/-2 years, mean+/-SEM) and in normotensive smokers (n=30, 39+/-1 years) before and 5, 10 and 15 minutes after smoking 1 cigarette (nicotine content: 0.9 mg). To evaluate the chronic effects of smoking, we compared the HR, brachial BP, PWVs, ABI and carotid intima-media thickness (IMT) between the normotensive smokers and nonsmokers (n=32, 37+/-1 years), and also between the hypertensive smokers and nonsmokers (n=21, 48+/-2 years). RESULTS: Smoking induced significant acute increases of the HR, brachial BP and hfPWV in the normotensive and hypertensive smokers (p<0.05), and smoking also induced significant acute increases in the faPWV and ankle systolic BP in the hypertensive smokers (p<0.05). The ABI, hcPWV and hbPWV in both groups, and the faPWV of the normotensives were not changed after smoking 1 cigarette (p>0.05). The magnitude of the increase in the HR, brachial BP and hfPWV after smoking were not different between the hypertensive and normotensive smokers. There was no significant differences (p>0.05) between the chronic normotensive smokers and the nonsmokers, and also between the hypertensive smokers and the non-smokers. CONCLUSION: Smoking acutely increased the HR, brachial BP and aortic stiffness in hypertensive smokers and normotensive smokers, and it had a more significant impact on the femoral arterial stiffness in the hypertensive smokers than in the normotensive smokers. However there were no significant chronic effects of smoking on the hemodynamics, arterial stiffness and carotid IMT. Our findings suggest that the acute increase in aortic and femoral arterial stiffness after smoking may contribute to the increased incidence of adverse cardiovascular events in smokers with hypertension.
Ankle ; Ankle Brachial Index ; Blood Pressure ; Carotid Intima-Media Thickness ; Heart Rate ; Hemodynamics* ; Humans ; Hypertension* ; Incidence ; Male ; Mechanics ; Pulse Wave Analysis ; Smoke* ; Smoking* ; Tobacco Products ; Vascular Stiffness

There has been a long-known association between high dietary sodium intake and hypertension, as well as the increased risk of cardiovascular disease. Reduction of sodium intake is a major challenge for public health. Recently, there have been several controversial large population-based studies regarding the current recommendation for dietary sodium intake. Although these studies were performed in a large population, they aroused controversies because they had a flaw in the study design and methods. In addition, knowledge of the advantages and disadvantages of the methods is essential in order to obtain an accurate estimation of sodium intake. I have reviewed the current literatures on the association between sodium intake and cardiovascular events, as well as the methods for the estimation of sodium intake.
Cardiovascular Diseases ; Hypertension ; Public Health ; Sodium* ; Sodium, Dietary ; Urine Specimen Collection

No abstract available.
Sodium

Sodium intake reduction has been emphasized because sodium adversely impacts health, especially blood pressure (BP), and the cardiovascular (CV) disease risk. However, data obtained from several cohort studies have raised questions regarding the effects of high sodium intake on BP and the CV disease risk. In the present study, we systematically reviewed the literature to evaluate these associations. Studies showing negative associations between urine sodium and BP and CV outcomes relied on estimated 24-hour urine sodium from spot urine that is inappropriate for determining sodium intake at an individual level. Furthermore, controversy about the association between 24-hour urine sodium and BP may have been caused by different characteristics of study populations, such as age distribution, ethnicity, potassium intake and the inclusion of patients with hypertension, the different statistical methods and BP measurement methods. Regarding the association between sodium intake and the CV disease risk, studies showing negative or J- or U-shaped associations used a single baseline measurement of 24-hour urine sodium in their analyses. However, recent studies that employed average of subsequently measured 24-hour urine sodium showed positive, linear associations between sodium intake and CV outcomes, indicating that controversies are caused by the different sodium intake measurement methods and analytic designs. In conclusion, the study shows that positive associations exist between sodium intake and BP, CV outcomes, and mortality, and that the argument that reducing sodium intake is dangerous is invalid. Sodium intake reduction should be recommended to all, and not limited to patients with hypertension or CV disease.

BACKGROUND: The major risk factors such as hypercholesterolemia, hypertension, diabetes melitus and cigarrete smoking have not been studied in an attempt to provide a composition of major risk factors in Korea. Also we have met with some patients without major risk factors. METHODS: A Retrospective Study was done on 160 patients of acute myocardial infarction who had been admitted to National Medical Center within 48 hours from onset, from January 1948 to December 1992 and studied on major risk factors of acute myocardial infarction. RESULTS: 1) Among major risk factors, smoking was found in 50%, hypertension in 49%, diabetes in 25% and hypercholesterolemia in 21%. 2) The percentage of patients without major risk factors was 19%. 3) Among major risk factors, hypertension, hypercholesterolemia and diabetes were increasing tendencies, recentely. CONCLUSION: Some patients with acute myocardial infarction don't have any major risk factors. Also hypertension, hypercholesterolemia and diabetes were increasing tendencies. So further study for other risk factors is needed and preventive management should require a commitment to behavior modification and alteration in life-style.
Behavior Therapy ; Humans ; Hypercholesterolemia ; Hypertension ; Korea ; Myocardial Infarction* ; Retrospective Studies ; Risk Factors* ; Smoke ; Smoking

BACKGROUND: We compared brachial-ankle pulse wave velocity (baPWV) measured by a simple oscillometric method with heart-carotid (hc) and heart-femoral (hf) PWVs measured by a conventional tonometic method. METHODS: Using an automatic waveform analyzer, we measured hcPWV, hfPWV and baPWV simultaneously. The subjects comprised 82 healthy subjects (normal group), 229 subjects without coronary artery disease (CAD) but with hypertension, diabetes, hypercholesterolemia, low HDL-cholesterol, smoking, or obesity (risk group), and 106 patients with coronary artery disease (CAD group). In 30 subjects, reproducibility of PWVs were determined. RESULTS: Pearson's correlation coefficients of intraobserver reproducibility of hcPWV, hfPWV and baPWV were r=0.855, r=0.912 and r=0.976, respectively (p<0.001 for all). The corresponding coefficients of variation (CV) were 4.5%, 4.5% and 2.6%. Pearson's correlation coefficients of interobserver reproducibility of hcPWV, hfPWV and baPWV were r=0.751, r=0.802 and r=0.972, respectively (p<0.001 for all). The corresponding CV were 7.8%, 5.8% and 3.3%. baPWV correlated well with hcPWV and hfPWV (r=0.457 and 0.640, respectively, p<0.001 for both). In normal and risk groups, age, sex and hypertension were major independent factors affecting hcPWV, hfPWV and baPWV. PWVs were increased according to the number of risk factors (p<0.001 for all). In CAD group, hfPWV was higher in patients with 3 vessel disease than those with 1+2 vessel disease (p=0.024). hcPWV, hfPWV and baPWV did not differ between risk and CAD groups in the age of 50 to 69 (p=NS for all). CONCLUSION: baPWV has good reproducibility and correlates acceptably with hcPWV and hfPWV. This simple measurement of baPWV is useful for screening of arterial stiffness.
Atherosclerosis ; Blood Flow Velocity ; Coronary Artery Disease ; Coronary Disease ; Humans ; Hypercholesterolemia ; Hypertension ; Mass Screening ; Obesity ; Pulse Wave Analysis* ; Risk Factors ; Smoke ; Smoking ; Vascular Stiffness

BACKGROUND AND OBJECTIVES: Even short-term treatment with angiotensin converting enzyme inhibitor in essential hypertension has been known to improve left ventricular (LV) diastolic function, LV hypertrophy (LVH), and aortic stiffness. The purpose of this study was to examine the effects of angiotensin II receptor antagonist (Losartan) on LV diastolic function, LVH, and aortic stiffness in essential hypertension. MATERIALS AND METHODS: Twenty-three hypertensive patients who were aged over 50 years, previously untreated, and without cardiac, renal, neurologic disease, or diabetes, were studied. Before and 12 weeks after monotherapy with Losartan 50 mg q.d., (1) supine arterial blood pressure by sphygmomanometry, (2) interventricular septum and LV posterior wall thickness, and LV end-diastolic dimension by M-mode echocardiography, (3) mitral peak E and A wave velocity by doppler echocardiography, (4) pulse wave velocity (PWV) in the descending aorta from aortic arch to the bifurcation by doppler echocardiography, were done. RESULTS: Twelve weeks after treatment, systolic blood pressure was lowered from 168.2+/-3.5 mmHg to 142.9+/-2.9 mmHg (p<0.05), diastolic blood pressure from 98.52.4 mmHg to 87.51.3 mmHg (p<0.05). Peak E/A ratio was increased from 0.75+/-0.04 to 0.82+/-0.04 (p<0.05). LV mass was decreased from 267.5+/-15.8 g to 235.6+/-12.6 g (p<0.05), and LV mass index from 166.8+/-8.0 g/m2 to 146.9+/-6.0 g/m2 (p<0.05). However, there were no significant change in PWV (from 7.18+/-0.10 m/sec to 7.23+/-0.30 m/sec, p>0.05), compliance (from 1.31+/-0.04 to 1.34+/-0.12, p>0.05), and compliance index (from 0.16+/-0.01 to 0.15+/-0.01, p>0.05). CONCLUSION: Short-term treatment with Losartan decreases blood pressure, improves LV diastolic function and LVH, but not aortic stiffness.
Angiotensin II* ; Angiotensins* ; Aorta, Thoracic ; Arterial Pressure ; Blood Pressure ; Compliance ; Echocardiography ; Echocardiography, Doppler ; Humans ; Hypertension ; Hypertrophy ; Losartan* ; Peptidyl-Dipeptidase A ; Pulse Wave Analysis ; Receptors, Angiotensin ; Vascular Stiffness* ; Ventricular Function, Left*

Behcet's disease (BD) is a systemic vasculitis involving diverse sizes of arteries and veins. We performed this study to evaluate the vascular changes by assessment of the arterial stiffness and intima-media thickness (IMT) of carotid artery in Korean patients with BD. Forty-one patients with BD and age-, and sex-matched 53 healthy subjects were recruited in this study. Carotid arterial stiffness and IMT were assessed by using high-resolution B-mode ultrasonography. Arterial stiffness parameters such as carotid arterial distensibility coefficient, stiffness index, and incremental elastic modulus (E(inc)) were significantly increased in BD patients compared with those in healthy subjects, but not in IMT. Positive relationship was noted between age and IMT, whereas age of onset was significantly associated with arterial stiffness in BD. This finding suggests impaired endothelial function before visible structural changes of arterial wall in BD. Age and age of onset may be an independent risk factor for carotid IMT and arterial stiffness, respectively. Further studies in more large populations are required to confirm our results.
Adolescent ; Adult ; Age Factors ; Arteries/pathology ; Behcet Syndrome/*diagnosis/*pathology ; Carotid Arteries/*pathology ; Carotid Artery Diseases/pathology ; Case-Control Studies ; Female ; Humans ; Korea ; Male ; Middle Aged ; Tunica Intima/pathology ; Tunica Media/pathology

One of the most important therapeutic targets of current cardiology practice is to determine optimal strategies for the minimization of myocardial necrosis and optimization of cardiac repair following an acute myocardial infarction. Myocardial necrosis after acute myocardial infarction induces complement activation and free radical generation, triggering a cytokine cascade initiated by tumor necrosis factor-alpha (TNF-alpha) release. When reperfusion of the infarcted area is initiated, intense inflammation follows. Chemokines, cytokines and the complement system play an important role in recruiting neutrophils in the ischemic and reperfused myocardium. Cytokines promote adhesive interactions between leukocytes and endothelial cells, resulting in transmigration of inflammatory cells into the site of injury. The recruited neutrophils have potent cytotoxic effects through the release of proteolytic enzymes, and they interact with adhesion molecules on cardiomyocytes. In spite of the potential injury, reperfusion enhances cardiac repair; this may be related to the inflammatory response. Monocyte chemoattractant protein (MCP)-1 is upregulated in reperfused myocardium and can induce monocyte recruitment in the infarcted area. Monocyte subsets play a role in phagocytosis of dead cardiomyocytes and in granulation tissue formation. In addition, the transforming growth factor (TGF)-beta plays a crucial role in cardiac repair by suppressing inflammation. Resolution of inflammatory infiltration, containment of inflammation and the reparative response affecting the infarcted area are essential for optimal infarct healing. Here, we review the current literature on the inflammatory response and cardiac repair after myocardial infarction.
Adhesives ; Cardiology ; Chemokines ; Complement Activation ; Complement System Proteins ; Containment of Biohazards ; Cytokines ; Endothelial Cells ; Granulation Tissue ; Inflammation ; Leukocytes ; Monocytes ; Myocardial Infarction ; Myocardium ; Myocytes, Cardiac ; Necrosis ; Neutrophils ; Peptide Hydrolases ; Phagocytosis ; Reperfusion ; Reperfusion Injury ; Transforming Growth Factors ; Tumor Necrosis Factor-alpha ; Ventricular Remodeling