Peripheral atherosclerosis evaluation through ultrasound: A promising diagnostic tool for coronary artery disease.

Effective treatment, but also proper diagnosis of cardiovascular diseases, remains a major challenge in everyday practice. A quick, safe, and economically acceptable non-invasive procedure should play a leading role in cardiovascular risk assessment before invasive diagnostics is performed. The staging of subclinical atherosclerosis may help in further clinical decisions. Safe, widely available, and relatively inexpensive, ultrasonography is a promising examination that should find wider application in clinical practice. The latest ESC guidelines emphasize the usefulness of carotid ultrasound in the diagnosis of coronary artery disease (CAD) and subclinical assessment of atherosclerosis, which help to determine the level of cardiovascular risk. Ultrasound examination of peripheral arteries, especially superficial vessels such as the femoral arteries, is quite easy, quick, and accurate. Other vascular beds, such as iliac and renal, are more demanding to examine, but can also provide valuable information. This review summarizes important studies comparing the severity of atherosclerosis in ultrasound-visible vascular beds in patients with established CAD. We especially emphasize the benefits of the combined assessment of atherosclerosis features, which were characterized by high sensitivity and specificity in the diagnosis of CAD and other serious cardiovascular diseases.

Atrial fibrillation does not affect ankle-brachial index measured using the Doppler method.

Atrial fibrillation may affect blood pressure measurements. The ankle-brachial index (ABI) is a ratio of systolic blood pressure measured on the lower and upper limbs that may also be affected by arrhythmia. The purpose of the study was to investigate whether atrial fibrillation influenced ABI results. Ninety-nine patients (age 66.6±11 years, 63 males and 36 females) who underwent electrical cardioversion of atrial fibrillation were investigated. ABI measurements using the Doppler method were performed on both lower extremities before and after electrical cardioversion. Measurements were repeated three times and then averaged. The ABI using both lower limbs was lower before electrical cardioversion than after restoration to sinus rhythm (right side: 1.132 (1.065-1.210) during atrial fibrillation vs. 1.179 (1.080-1.242) in sinus rhythm, P=0.019; left side: 1.142 (1.075-1.222) during atrial fibrillation vs. 1.170 (1.098-1.255) in sinus rhythm, P=0.011). However, the upper 95% confidence interval (CI) margins for the median differences in ABI were 0.045 and 0.040 for right and left, respectively, suggesting that the observed difference was clinically insignificant. There was a significant correlation between measurements obtained before and after electrical cardioversion on both lower limbs (r=0.61, P<0.001 and r=0.67, P<0.001). The Bland-Altman plot showed good agreement between measurements performed using the Doppler method during atrial fibrillation and sinus rhythm. Study results showed that atrial fibrillation did not have a clinically important effect on ABI measurements.

The effect of hyperoxia on central blood pressure in healthy subjects.

INTRODUCTION: Hyperoxia increases total peripheral resistance by acting locally but also inhibits the activity of carotid body chemoreceptors. We studied the effect of hyperoxia on central pressure in normotensive subjects. MATERIAL AND METHODS: Medical air followed by 100% oxygen was provided to 19 subjects (12/7 female/male, age 28.2 ±1.1 years) for 15 min through a non-rebreather mask. Central blood pressure was then measured using applanation tonometry. RESULTS: After the first 2 min of hyperoxia, heart rate decreased significantly (65 ±2.6 beats/min vs. 61 ±2.1 beats/min, p = 0.0002). Peripheral and central blood pressure remained unchanged, while hemoglobin oxygen saturation and subendocardial viability ratio index increased (97 ±0.4% vs. 99 ±0.2%, p = 0.03; 168 ±8.4% vs. 180 ±8.2%, p = 0.009). After 15 min of 100% oxygen ventilation, heart rate and peripheral and central blood pressures remained unchanged from the first 2 min. The augmentation index, augmentation pressure and ejection duration increased as compared to baseline values and those obtained at 2 min (-5.1 ±2.9% vs. -1.2 ±2.6%, p = 0.005 and -4.6 ±2.7% vs. -1.2 ±2.6%, p = 0.0015; -1.3 ±0.7 mm Hg vs. -0.2 ±1.2 mm Hg, p = 0.003 and -1.1 ±0.7 mm Hg vs. -0.2 ±1.2 mm Hg, p = 0.012; 323 ±3.6 ms vs. 330 ±3.5 ms, p = 0.0002 and 326 ±3.5 ms vs. 330 ±3.5 ms, p = 0.021, respectively). CONCLUSIONS: The present study shows that hyperoxia does not affect central blood pressure in young healthy subjects and may improve myocardial blood supply estimated indirectly from applanation tonometry.

Electric cardioversion of atrial fibrillation resulting in pulmonary oedema in patient with apical hypertrophic cardiomyopathy.

The direct-current electric shock is considered to be safe treatment of arrhythmias and rarely leads to serious hemodynamic complications. A 62-year-old patient was admitted to the hospital due to a first symptomatic episode of atrial fibrillation. Patient was diagnosed with apical hypertrophic cardiomyopathy 20 years ago. Transoesophageal echocardiography was performed to exclude an atrial thrombus followed by electrical cardioversion with restoration of sinus rhythm. After 6 hours symptoms of pulmonary oedema developed. The patient's condition improved after furosemide administration. As the possible cause of the oedema, inotropic effect of administered propafenone and atrial stunning were considered. The atria seem to be responsible for important part of forward cardiac output even during AF, especially in cardiomyopathies. Contractility deterioration of the left atrium (stunning) along with earlier resumption of the right atrium contractile function could be associated with hemodynamic instability causing pulmonary oedema in subjects with hypertrophied myocardium. It is necessary to take into consideration the atrial function while administrating antiarrhythmic drugs, especially those with negative inotropic effect.

Acute clenbuterol overdose manifestations in a suicide attempt--a case report.

A 30-year-old man was admitted to the intensive care unit after a suicide attempt with respiratory difficulties, tremor, sinus tachycardia and significant hypokalemia. On examination, the patient was lucid, fully conscious and did not exhibit positive symptoms. Sings were not typical for overdosing olanzapine, alprazolam and alcohol as declared by the patient. Additional anamnesis revealed high doses of ingested clenbuterol, a selective ß2-adrenergic agonist. Due to its anabolic and lipolytic properties, clenbuterol has become a commonly abused drug in bodybuilding industry and is not routinely detected by toxicology screens. This is the first known report of suicide attempt by clenbuterol overdosing.

Deactivation of carotid body chemoreceptors by hyperoxia decreases blood pressure in hypertensive patients.

Previous studies have shown that hyperoxia-induced deactivation of carotid body chemoreceptors reduces sympathetic activity in hypertensive patients but it does not affect blood pressure. The maintenance of blood pressure can be explained by the direct, vasoconstrictive effect of hyperoxia, which offsets diminished sympathetic activity. This study compares the effect of acute hyperoxia on hemodynamic parameters between hypertensive and normotensive subjects. Twelve males with hypertension (age 39.4±2.4 years; body mass index 27.4±1.1 kg m(-2)) and 11 normotensive males (age 39.9±2.7 years; body mass index 25.4±0.7 kg m(-2)) received, via non-rebreathing mask ventilation, ambient air, followed by 100% oxygen for 20 min. The stroke volume, heart rate, cardiac output, blood pressure, total peripheral resistance, respiratory rate, baroreceptor control of heart rate and oxygen saturation were recorded continuously. Several 30 s periods were analyzed before, during and after inducing hyperoxia. At baseline, the hypertensive subject's blood pressure was higher and their baroreflex control of heart rate was lower when compared with the normotensive control group. After the first 30 s of hyperoxia, systolic, diastolic and mean blood pressures, as well as the total peripheral resistance, decreased significantly in hypertensives but not in normotensives. After 20 min of 100% oxygen ventilation, systolic and mean blood pressures and total peripheral resistance was increased in hypertensive patients, and the cardiac output and stroke volume had decreased in both groups. The results of this study confirm that deactivation of carotid body chemoreceptors can acutely decrease blood pressure in humans.

Individuals with high-normal blood pressure have different metabolic and haemodynamic characteristics to those with optimal blood pressure.

BACKGROUND: The ESH classification of blood pressure includes the high-normal blood pressure (HNBP) category, which is within normal limits but associated with increased cardiovascular (CV) risk. AIM: To identify additional CV risk factors and early signs of target organ damage in healthy individuals with HNBP. METHODS: Healthy volunteers (n = 74) with optimal blood pressure or HNBP were compared with respect to metabolic and haemodynamic parameters. RESULTS: The HNBP was associated with higher serum uric acid (333.1 ± 65.4 vs 267.7 ± 65.4 µmol/L, p < 0.05) and glucose (4.7 ± 0.3 vs 4.5 ± 0.3 mmol/L, p < 0.01) concentrations, intima-media thickness (0.39 ± 0.06 vs 0.36 ± 0.04 mm, p < 0.05), systemic vascular resistance index (2,678.2 ± 955.9 vs 1,930.2 ± 625.5 dyn x s x m(2)/cm(5), p < 0.001), lower total arterial compliance index (1.04 ± 0.42 vs 1.44 ± 0.48 mL/[mm Hg x m(2)], p < 0.01) and baroreflex sensitivity (14.2 ± 3.8 vs 18.0 ± 8.8 mm Hg(2)/Hz, p = 0.05). CONCLUSIONS: The observed differences in metabolic and haemodynamic profile in HNBP may adversely affect CV risk in these individuals.

Tonic activity of carotid body chemoreceptors contributes to the increased sympathetic drive in essential hypertension.

Carotid chemoreceptors provoke an increase in muscle sympathetic nerve activation (MSNA) in response to hypoxia; they are also tonically active during normoxic breathing. The contribution of peripheral chemoreceptors to sympathetic activation in hypertension is incompletely understood. The aim of our study was to investigate the effect of chemoreceptor deactivation on sympathetic activity in untreated patients with hypertension. A total of 12 untreated hypertensive males and 11 male controls participated in this randomized, crossover, placebo-controlled study. MSNA, systolic blood pressure(BP), diastolic BP, heart rate (HR), electrocardiogram, hemoglobin oxygen saturation (Sat%) and respiratory movements were measured during repeated 10-min periods of respiration with 100% oxygen or 21% oxygen in a blinded fashion. Compared with controls, hypertensives had higher resting MSNA (38 ± 10 vs. 29 ± 0.9 burst per min, P<0.05), systolic BP (150 ± 12 vs. 124 ± 10 mm Hg, P< 0.001) and diastolic BP (92 ± 10 vs. 77 ± 9 mm Hg, P<0.005). Breathing 100% oxygen caused significant decrease in MSNA in hypertensive patients (38 ± 10 vs. 26 ± 8 burst per min and 100 ± 0 vs. 90 ± 10 arbitrary units, P<0.05) and no change in controls (29 ± 9 vs. 27 ± 7 burst per min and 100 ± 0 vs. 96 ± 11 arbitrary units). BP, respiratory frequency and end tidal CO(2) did not change during chemoreceptor deactivation with hyperoxia. HR decreased and Sat% increased in both the study groups. These results confirm the role of tonic chemoreceptor drive in the development of sympathetic overactivity in hypertension.

Simvastatin reduces sympathetic activity in men with hypertension and hypercholesterolemia.

Beyond their hypolipidemic effect, statins reduce cardiovascular risk in hypertensive subjects via various mechanisms; one suggested mechanism is that they reduce sympathetic activity. We investigated the hypothesis that simvastatin decreased muscle sympathetic nerve activity (MSNA) in 31 hypertensive subjects with hypercholesterolemia (aged 38.7 ± 10 years). In this randomized, placebo-controlled, double-blinded study, patients were treated with simvastatin (40 mg day(-1); n=15) or placebo (n=16) for 8 weeks. Before and after treatment, we measured MSNA, blood pressure and heart rate. Baroreceptor control of the heart rate, or baroreceptor sensitivity (BRS), was computed by the sequence method, a cross-analysis of systolic blood pressure and the electrocardiogram R-R interval. Blood samples were tested for plasma levels of catecholamines, neuropeptide Y, aldosterone, endothelin and renin activity. Simvastatin significantly reduced MSNA (from 36.5 ± 5 to 27.8 ± 6 bursts per min, P=0.001), heart rate (from 77 ± 6.7 to 71 ± 6.1 beats per min, P=0.01) and both total and low-density lipoprotein cholesterol (from 249 ± 30.6 to 184 ± 28.3 mg dl(-1), P=0.001 and from 169 ± 30.6 to 117 ± 31.2 mg dl(-1), P=0.01, respectively). Simvastatin also improved BRS (from 10.3 ± 4.1 to 17.1 ± 4.3 ms per mm Hg, P=0.04). No changes were observed in systolic or diastolic blood pressures, or in plasma levels of catecholamines, neuropeptide Y, endothelin, aldosterone and renin activity. After simvastatin therapy, MSNA and BRS were inversely related (r=-0.94, P<0.05). In conclusion, we found that, in patients with hypertension and hypercholesterolemia, simvastatin reduced MSNA, and this was related to increased baroreceptor sensitivity.

Cardiotoxicity of the anticancer therapeutic agent bortezomib.

Recent case reports provided alarming signals that treatment with bortezomib might be associated with cardiac events. In all reported cases, patients experiencing cardiac problems were previously or concomitantly treated with other chemotherapeutics including cardiotoxic anthracyclines. Therefore, it is difficult to distinguish which components of the therapeutic regimens contribute to cardiotoxicity. Here, we addressed the influence of bortezomib on cardiac function in rats that were not treated with other drugs. Rats were treated with bortezomib at a dose of 0.2 mg/kg thrice weekly. Echocardiography, histopathology, and electron microscopy were used to evaluate cardiac function and structural changes. Respiration of the rat heart mitochondria was measured polarographically. Cell culture experiments were used to determine the influence of bortezomib on cardiomyocyte survival, contractility, Ca(2+) fluxes, induction of endoplasmic reticulum stress, and autophagy. Our findings indicate that bortezomib treatment leads to left ventricular contractile dysfunction manifested by a significant drop in left ventricle ejection fraction. Dramatic ultrastructural abnormalities of cardiomyocytes, especially within mitochondria, were accompanied by decreased ATP synthesis and decreased cardiomyocyte contractility. Monitoring of cardiac function in bortezomib-treated patients should be implemented to evaluate how frequently cardiotoxicity develops especially in patients with pre-existing cardiac conditions, as well as when using additional cardiotoxic drugs.

Atorvastatin reduces sympathetic activity and increases baroreceptor reflex sensitivity in patients with hypercholesterolaemia and systemic arterial hypertension.

BACKGROUND: Increased sympathetic activity might be related to pathogenesis of hypertension as well as to end organ damage. Animal studies suggest that statins decrease sympathetic activity and increase baroreceptor reflex sensitivity (BRS). AIM: To examine whether atorvastatin decreases muscle sympathetic nerve activity (MSNA) and BRS in hypercholesterolaemic and hypertensive patients. METHODS: Ten patients with essential hypertension and untreated hypercholesterolaemia (aged 43 +/- 12 years) and eight healthy subjects (aged 37 +/- 7 years) were enrolled in the study. In both groups the recordings of microneurography, ECG, blood pressure and BRS were performed twice, before and after 8 weeks during which the patients (but not controls) were treated with atorvastatin. RESULTS: Compared with controls, the patients had higher MSNA values (36.0 +/- 6.6 vs. 29.8 +/- 3.7 bursts/minute), mean BP levels (145.1 +/- 10 vs. 124.1 +/- 11.1 mmHg) and total cholesterol concentration (252.6 +/- 22.6 vs. 179.8 +/- 20.7 mg/dl) baseline values. Statin therapy resulted in a decrease of total cholesterol (252.6 +/- 22.0 vs. 173.8 +/- 26.2 mg/dl, p < 0.05) and MSNA (36.0 +/- 6.6 vs. 28.6 +/- 4.8 bursts/min, p < 0.05), whereas BRS values were increased (12.6 +/- 5.6 vs. 18.1 +/- 5.9 ms/mmHg, p < 0.05). Post-treatment BRS was inversely related to post-treatment MSNA (r = -0.73, p < 0.05). In the controls there were no changes in MSNA (29.8 +/- 3.7 vs. 28.9 +/- 2.9 bursts/min), BRS (11.9 +/- 5.0 vs. 13.1 +/- 4.8 ms/mmHg), total cholesterol, BP and heart rate between the first and the second measurement. CONCLUSION: Atorvastatin reduces MSNA and increases BRS in hypertensive and hypercholesterolaemic patients. Decrease in sympathetic activity may be the result of improvement of baroreceptor function by atorvastatin.

Descending aortic Doppler flow pattern in patients with proximal peripheral artery disease.

Midsystolic deceleration (notch) in pulmonary pulse-wave (PW) Doppler flow is a common finding in patients with pulmonary embolism. The possible mechanism involves early reflection of pressure wave from proximal embolic sites. The aim of this study was to evaluate with PW Doppler whether occlusion or significant stenosis in the distal aorta or iliac arteries might produce a similar midsystolic notch in descending aortic flow. Echocardiography was performed in 97 consecutive patients with severe peripheral artery disease (PAD) admitted for vascular surgery and in 41 controls. PW Doppler assessment of flow in the proximal descending aorta was recorded from the suprasternal window. After exclusion of 13 patients due to inadequate visualization, atrial fibrillation, or aortic aneurysm, 84 patients were analyzed. Diagnosis of midsystolic notch was made by an experienced echocardiographer blinded to the vascular status of patients. A midsystolic notch in the descending aorta was present in 43 of 49 patients (87.7%) with occlusion or with >70% stenosis in the aortoiliac segment, 6 of 35 (17.1%) patients with occlusion or significant stenosis distal to the external iliac artery, and 0 patient from the control group. Sensitivity of the midsystolic notch in the detection of aortoiliac disease in patients with PAD was 87.7% and specificity was 82.8%. In conclusion, midsystolic deceleration (notch) in the descending aortic Doppler waveform is characteristic for patients with significant proximal PAD. The possible mechanism involves arterial pressure wave reflection from the occlusion or significant stenosis in the aortoiliac segment.

The effect of enalapril and telmisartan on clinical and biochemical indices of sympathetic activity in hypertensive patients.

OBJECTIVE: To compare the effect of ARB and ACE inhibitor on sympathetic activity in 32 hypertensives. DESIGN AND METHODS: After a four-week wash-out period, patients were randomized to four weeks of therapy with enalapril or telmisrtan, with crossover to another drug for another four weeks. Blood pressure (BP), NPY, and catecholamine levels and HRV (frequency analysis) were measured during wash-out, in basal condition, and after postural stimulation test (PST). RESULTS: Both drugs significantly reduced BP and NPY as compared to initial values, while no differences in BP and NPY between drugs were observed. Increase in NPY during PST was significantly higher in the enalapril than in the telmisartan group and during the wash-out period. No differences between enalapril and telmisartan in plasma catecholamines were observed. Telmisartan decreased low frequency/high frequency ratio as compared to initial values and enalapril values. CONCLUSIONS: Despite similar BP control, telmisartan attenuated autonomic balance more effectively than enalapril.

Biomarker-based risk assessment model in acute pulmonary embolism.

AIMS: Despite growing interest in biomarkers application for risk evaluation in acute pulmonary embolism (APE), no decision-making levels have been defined. METHODS AND RESULTS: We developed a biomarker-based risk stratification in 100 consecutive, normotensive on admission, APE patients (35 males, 65 females, 62+/-18 years). On admission serum NT-proBNP and cardiac troponin T (cTnT) levels were assessed and echocardiography was performed. All-cause 40-day mortality was 15% and APE mortality was 8%. In univariable analysis, cTnT>0.07 microg/L predicted all-cause mortality, hazard ratio (HR) 9.2 (95% CI: 3.3-26.1, P<0.0001), and APE mortality, HR 18.1 (95% CI: 3.6-90.2, P=0.0004); similarly, NT-proBNP>7600 ng/L predicted all-cause and APE mortalities [HR 6.7 (95% CI: 2.4-19.0, P=0.0003) and 7.3 (95% CI: 1.7-30.6, P=0.007)]. NT-proBNP<600 ng/L indicated uncomplicated outcome. Multivariable analysis revealed that cTnT>0.07 microg/L was the most significant independent predictor, whereas NT-proBNP and systemic systolic blood pressure measured on admission and echocardiographic parameters were non-significant. APE mortality in patients with NT-proBNP> or =600 ng/L and cTnT> or =0.07 microg/L reached 33%. NT-proBNP<600 ng/L indicated group without deaths. APE mortality for patients with NT-proBNP> or =600 ng/L and cTnT<0.07 microg/L was 3.7%. Incorporation of echocardiographic data did not improve group selection. CONCLUSION: Simultaneous measurement of serum cTnT and NT-proBNP allows for precise APE prognosis. Normotensive patients on admission with cTnT> or =0.07 microg/L and NT-proBNP> or =600 ng/L are at high risk of APE mortality, whereas NTproBNP<600 ng/L indicates excellent prognosis.

[Comparison of the effect of nitroglycerine and pentaerithritol compositum on exercise time restricted by anginal pain or objective parameters of ischaemia in patients with stable angina]. / Porównanie wplywu nitrogliceryny i preparatu zlozonego pentaerythritol compositum w postaci podjezykowej na czas wystapienia dolegliwosci dlawicowych i obiektywnych wskazników niedokrwienia podczas wysilku fizycznego u chorych ze stabilna choroba niedokrwienna.

Short acting nitrates are commonly used to prevent the anginal pain. The purpose of the study was to compare antianginal efficacy of Pentaerythritol compositum (20 mg of pentaerythritol tetranitrate and 0.5 mg of nitroglicerine) and 0,5 mg of nitroglycerine. Twenty patients aged 45-75 years with stable angina were enrolled. Antianginal effectiveness was evaluated during treadmill test. Time to ischemic pain and/or electrocardiographic parameters of ischemia were measured. It was found that Pentaerythritol compositum was superior to nitroglycerine in preventing angina with the difference disappearing 60 minutes after drug administration. Both drugs were well tolerated. Achieved results show that Pentaerythritol compositum can be effective as antianginal drug in patients with stable angina.