Clear cell renal carcinoma metastases to the pancreas.

INTRODUCTION: To date, clear cell renal carcinoma (Grawitz tumour) remains the most frequent malignant tumour of the kidney in adults. It metastasises in more than 25% of cases, most frequently to the bones (osteolytic metastases), lungs, brain, liver, adrenal glands and the contralateral kidney. Metastases to the pancreas are rare and represent 1-4% of all malignant tumours of the pancreas. METHODS: This is a retrospective analysis of patients who were operated at the Department of Surgery in Pilsen between 2010 and 2018 for histologi-cally verified metastasis of clear cell carcinoma (Grawitz tumour) to the pancreas. RESULTS: We operated 12 patients (8 men and 4 women). The metastases appeared on average 8 years and 8 months following the primary urolo-gical surgery. The mean age of the male patients was 66.5 years and that of the female patients was 67.4 years. In our sample, the diagnostic specificity of the CT scan was 50%, the diagnostic specificity of endoscopic ultrasound (EUS) was 75% and subsequent EUS-guided fine needle aspiration biopsy performed in 100% of cases yielded a specificity of 75%. Resectability was 92%. The average length of hospitalisation was 11.5 days. Post-operative complications according to Clavien-Dindo were grade 1 in 66%, grade 2 in 1.25% and grade 5 in 8.3% of the cases. The 30-day post-operative mortality was 8.3% (one patient).  Conclusion: Clear cell renal carcinoma metastases to the pancreas are very rare. However, if radically removed, the patient has a good prognosis with regards to long-term survival.

Tracking Optical Welding through Groove Modes in Plasmonic Nanocavities.

We report the light-induced formation of conductive links across nanometer-wide insulating gaps. These are realized by incorporating spacers of molecules or 2D monolayers inside a gold plasmonic nanoparticle-on-mirror (NPoM) geometry. Laser irradiation of individual NPoMs controllably reshapes and tunes the plasmonic system, in some cases forming conductive bridges between particle and substrate, which shorts the nanometer-wide plasmonic gaps geometrically and electronically. Dark-field spectroscopy monitors the bridge formation in situ, revealing strong plasmonic mode mixing dominated by clear anticrossings. Finite difference time domain simulations confirm this spectral evolution, which gives insights into the metal filament formation. A simple analytic cavity model describes the observed plasmonic mode hybridization between tightly confined plasmonic cavity modes and a radiative antenna mode sustained in the NPoM. Our results show how optics can reveal the properties of electrical transport across well-defined metallic nanogaps to study and develop technologies such as resistive memory devices (memristors).

Active nanoplasmonic metamaterials.

Optical metamaterials and nanoplasmonics bridge the gap between conventional optics and the nanoworld. Exciting and technologically important capabilities range from subwavelength focusing and stopped light to invisibility cloaking, with applications across science and engineering from biophotonics to nanocircuitry. A problem that has hampered practical implementations have been dissipative metal losses, but the efficient use of optical gain has been shown to compensate these and to allow for loss-free operation, amplification and nanoscopic lasing. Here, we review recent and ongoing progress in the realm of active, gain-enhanced nanoplasmonic metamaterials. On introducing and expounding the underlying theoretical concepts of the complex interaction between plasmons and gain media, we examine the experimental efforts in areas such as nanoplasmonic and metamaterial lasers. We underscore important current trends that may lead to improved active imaging, ultrafast nonlinearities on the nanoscale or cavity-free lasing in the stopped-light regime.

Controlled storage and transfer of photonic space-time quantum-coherence in active quantum dot nanomaterials.

We demonstrate the potential of semiconductor quantum dot nanomaterials for solid-state based controllable quantum memories in which losses may be compensated by gain. The dynamic photonic quantum-coherence present in a quantum dot ensemble and generated by a coherent signal pulse is influenced and controlled by disorder, spectral detuning and the power of the pulse. We show that the high coupling of spatial and temporal degrees of freedom is a key requirement for coherence transfer and/or storage.

ECG-triggered skeletal muscle stimulation improves hemodynamics and physical performance of heart failure patients.

BACKGROUND: Muscular counterpulsation (MCP) was developed for circulatory assistance by stimulation of peripheral skeletal muscles. We report on a clinical MCP study in patients with and without chronic heart failure (CHF). METHODS AND RESULTS: MCP treatment was applied (30 patients treated, 25 controls, all under optimal therapy) for 30 minutes during eight days by an ECG-triggered, battery-powered, portable pulse generator with skin electrodes inducing light contractions of calf and thigh muscles, sequentially stimulated at early diastole. Hemodynamic parameters (ECG, blood pressure and echocardiography) were measured one day before and one day after the treatment period in two groups: Group 1 (9 MCP, 11 no MCP) with ejection fraction (EF) above 40% and Group 2 (21 MCP, 14 no MCP) below 40%. In Group 2 (all patients suffering from CHF) mean EF increased by 21% (p<0.001) and stroke volume by 13% (p<0.001), while end systolic volume decreased by 23% (p<0.001). In Group 1, the increase in EF (6%) and stroke volume (8%) was also significant (p<0.05) but less pronounced than in Group 2. Physical exercise duration and walking distance increased in Group 2 by 56% and 72%, respectively. CONCLUSIONS: Noninvasive MCP treatment for eight days substantially improves cardiac function and physical performance in patients with CHF.

[Liver cystadenoma with ovarian stroma--a case review]. / Cystadenom jater s ovariálním stromatem--kazuistika.

Cystadenoma with ovarian type of stroma is a rare liver tumor. Authors discuss diagnostic difficulties and troublesome therapy with potential complications at unfavourable central localization in the liver of 46 years old woman.

Micrometer size polarization independent depletion-type photonic modulator in Silicon On Insulator.

The trend in silicon photonics, in the last few years has been to reduce waveguide size to obtain maximum gain in the real estate of devices as well as to increase the performance of active devices. Using different methods for the modulation, optical modulators in silicon have seen their bandwidth increased to reach multi GHz frequencies. In order to simplify fabrication, one requirement for a waveguide, as well as for a modulator, is to retain polarisation independence in any state of operation and to be as small as possible. In this paper we provide a way to obtain polarization independence and improve the efficiency of an optical modulator using a V-shaped pn junction base on the natural etch angle of silicon, 54.7 deg. This modulator is compared to a flat junction depletion type modulator of the same size and doping concentration.

ECG-triggered muscular counterpulsation for treatment of low cardiac output.

BACKGROUND: Skeletal muscular counterpulsation (MCP) has been used as a new noninvasive technique for treatment of low cardiac output. The MCP method is based on ECG-triggered skeletal muscle stimulation. The purpose of the present study was to evaluate acute hemodynamic changes induced by MCP in the experimental animal. METHODS: Eight anaesthetized pigs (43+/-4 kg) were studied at rest and after IV â-blockade (10 mg propranolol) before and after MCP. Muscular counterpulsation was performed on both thighs using trains (75 ms duration) of multiple biphasic electrical impulses with a width of 1 ms and a frequency of 200 Hz at low (10 V) and high (30 V) amplitude. ECG-triggering was used to synchronize stimulation to a given time point. LV pressure-volume relations were determined using the conductance catheter. After baseline measurements, MCP was carried out for 10 minutes at low and high stimulation amplitude. The optimal time point for MCP was determined from LV pressure-volume loops using different stimulation time points during systole and diastole. Best results were observed during end-systole and, therefore, this time point was used for stimulation. RESULTS: Under control conditions, MCP was associated with a significant decrease in pulmonary vascular resistance (-18%), a decrease in systemic vascular resistance (-11%) and stroke work index (-4%), whereas cardiac index (+2%) and ejection fraction (+6%) increased slightly. Pressure-volume loops showed a leftward shift with a decrease in end-systolic volume. After â-blockade, cardiac function decreased (HR, MAP, EF, dP/dt max), but it improved with skeletal muscle stimulation (HR +10% and CI +17%, EF +5%). There was a significant decrease in pulmonary (-19%) and systemic vascular resistance (-29%). CONCLUSIONS: In the animal model, ECG-triggered skeletal muscular counterpulsation is associated with a significant improvement in cardiac function at baseline and after IV â-blockade. Thus, MCP represents a new, non-invasive technique which improves cardiac function by diastolic compression of the peripheral arteries and veins, with a decrease in systemic vascular resistance and increase in cardiac output.

Ultrafast nonlinear dynamics of whispering-gallery mode micro-cavity lasers.

We explore the ultrafast spatio-temporal dynamics of whispering-gallery micro-cavity lasers. To model the dynamics of the nonlinear whispering-gallery modes we develop a three-dimensional Finite-Difference Time-Domain modelling framework based on the spin and therefore optical polarisation resolved Maxwell-Bloch equations. The numerical algorithm brings together a real value form of the optical Bloch equations with the curl part of Maxwell's equations. The Hamiltonian of the two-level system contains either linear or circular polarised transitions. In cylindrical micro-cavity lasers the coherent, nonlinear emission process leads to ultrafast fan-like rotational phase dynamics of the degenerate whispering-gallery modes. This rotation is shown to be arrested in gear-shaped micro-cavity lasers followed by an over-damped relaxation oscillation.

Improved neo-endothelialization of small diameter ePTFE grafts with titanium coating.

BACKGROUND: Patency of small synthetic bypass grafts is inferior compared to autologous grafts for revascularization procedures. Titanium coating of foreign surfaces has shown to decrease thrombogenicity, enhance biocompatibility and promote adhesion of endothelial cells. The aim of this study was to test the effect of titanium coating of small diameter ePTFE grafts on short term patency, neo-endothelialization and neointimal proliferation. METHODS: Bilateral carotid graft interposition was performed in 5 pigs with uncoated (n=5) and titanium-coated (n=5) ePTFE grafts (internal diameter=4 mm, length=5 cm), thus each pig served as its own control. At the end of the study (30 +/- 3 days), patency and stenosis severity was assessed by carotid angiography. Animals were sacrificed and grafts were excised for histology and scanning electron microscopy. Morphometry of histologic sections was carried out to determine neointimal proliferation and percentage of neo-endothelial coverage. RESULTS: Patency rate was 80% for uncoated and titanium-coated grafts. Quantitative angiography did not show any significant difference in lumen size between two groups. Morphometry revealed a significantly higher cellular coverage with CD31 positive endothelial cells for titanium-coated (84 +/- 19%) than uncoated grafts (48 +/- 26%, p<0.001). There was a non significant trend (p=0.112) towards increased neointimal proliferation in titanium-coated (94 +/- 61 micron2/micron) compared to uncoated grafts (60 +/- 57 micron2/micron). CONCLUSIONS: Patency rate in uncoated and titanium-coated ePTFE grafts is similar at one month. However, titanium coated grafts show a significant improvement in neo-endothelialization compared to uncoated grafts.

Effect of NO donors on LV diastolic function in patients with severe pressure-overload hypertrophy.

BACKGROUND: Previous experimental studies have shown that nitric oxide (NO) modulates cardiac function by an abbreviation of systolic contraction and an enhancement of diastolic relaxation. However, the response to NO donors of patients with severe pressure-overload hypertrophy and diastolic dysfunction is unknown. METHODS AND RESULTS: Intracoronary NO donors were given to 17 patients with severe aortic stenosis. A dose-response curve was obtained with nitroglycerin (30, 90, and 150 microg) in 11 patients and sodium nitroprusside (1, 2, and 4 microg/min) in 6. Left ventricular (LV) high-fidelity pressure measurements with simultaneous LV angiograms were performed at baseline and after the maximal dose of NO. The dose-response curve for intracoronary NO donors showed a marked fall in LV end-diastolic pressure, from 23 to 14 mm Hg (-39%; P<0.0001), whereas LV peak systolic pressure fell only slightly, from 206 to 196 mm Hg (-4%; P<0.01). End-diastolic chamber stiffness decreased from 0.12 to 0.07 mm Hg/mL (P<0.0001) and end-systolic stiffness from 1.6 to 1.3 mm Hg/mL (P<0.01). Heart rate, right atrial pressure, LV ejection fraction, the time constant of isovolumic pressure decay (tau), and LV filling rates remained unchanged. CONCLUSIONS: In patients with severe pressure-overload hypertrophy, intracoronary NO donors exert a marked decrease in LV end-diastolic pressure without affecting LV systolic pump function. Thus, the hypertrophied myocardium appears to be particularly susceptible to NO donors, with a marked improvement in diastolic function.

Alterations in the local myocardial motion pattern in patients suffering from pressure overload due to aortic stenosis.

BACKGROUND: MR tissue tagging allows the noninvasive assessment of the locally and temporally resolved motion pattern of the left ventricle. Alterations in cardiac torsion and diastolic relaxation of the left ventricle were studied in patients with aortic stenosis and were compared with those of healthy control subjects and championship rowers with physiological volume-overload hypertrophy. METHODS AND RESULTS: Twelve aortic stenosis patients, 11 healthy control subjects with normal left ventricular function, and 11 world-championship rowers were investigated for systolic and diastolic heart wall motion on a basal and an apical level of the myocardium. Systolic torsion and untwisting during diastole were examined by use of a novel tagging technique (CSPAMM) that provides access to systolic and diastolic motion data. In the healthy heart, the left ventricle performs a systolic wringing motion, with a counterclockwise rotation at the apex and a clockwise rotation at the base. Apical untwisting precedes diastolic filling. In the athlete's heart, torsion and untwisting remain unchanged compared with those of the control subjects. In aortic stenosis patients, torsion is significantly increased and diastolic apical untwisting is prolonged compared with those of control subjects or athletes. CONCLUSIONS: Torsional behavior as observed in pressure- and volume-overloaded hearts is consistent with current theoretical findings. A delayed diastolic untwisting in the pressure-overloaded hearts of the patients may contribute to a tendency toward diastolic dysfunction.

alpha-adrenergic coronary vasoconstriction and myocardial ischemia in humans.

The use of quantitative coronary angiography, combined with Doppler and PET, has recently been directed at the study of alpha-adrenergic coronary vasomotion in humans. Confirming prior animal experiments, there is no evidence of alpha-adrenergic coronary constrictor tone at rest. Again confirming prior experiments, responses to alpha-adrenoceptor activation are augmented in the presence of coronary endothelial dysfunction and atherosclerosis, involving both alpha(1)- and alpha(2)-adrenoceptors in epicardial conduit arteries and microvessels. Such augmented alpha-adrenergic coronary constriction is observed during exercise and coronary interventions, and it is powerful enough to induce myocardial ischemia and limit myocardial function. Recent studies indicate a genetic determination of alpha(2)-adrenergic coronary constriction.

Stent coating with titanium-nitride-oxide for reduction of neointimal hyperplasia.

BACKGROUND: Coronary stents prevent constrictive arterial remodeling but stimulate neointimal hyperplasia. Stainless steel induces a metallic foreign body reaction, which is absent for titanium. The hypothesis of the present study was that titanium renders the stent surface biologically inert, with reduced platelet and fibrinogen binding. METHODS AND RESULTS: Twelve pigs were instrumented with a stainless steel and 2 titanium-nitride-oxide-coated stents (TiNOX 1, ceramic; TiNOX 2, metallic). Animals were restudied after 6 weeks. Histological specimens of stented segments were analyzed by digital morphometry. Platelet adhesion and fibrinogen binding studies were performed in the perfusion chamber. Under in vitro conditions, TiNOX 1 showed reduced platelet adhesion (65+/-3%) compared with TiNOX 2 (72+/-5%; P<0.05) and stainless steel (71+/-4%; P<0.05). Platelet adhesion 48 hours after incubation with human plasma, however, was not different between TiNOX 1 (17+/-3%) and 2 (15+/-3%) but was significantly higher with stainless steel (23+/-2%; P<0.05). Fibrinogen binding was significantly reduced with TiNOX 2 (54+/-3%) compared with TiNOX 1 (82+/-4%, P<0.05) or stainless steel (100%, P<0.05). Histomorphometry revealed a significantly larger neointimal area in stainless steel (2.61+/-1.12 mm(2)) than in TiNOX 1-coated (1.47+/-0.84 mm(2), P<0.02) or TiNOX 2-coated (1.39+/-0.93 mm(2), P<0.02) stents. The reductions were 44% and 47%, respectively. CONCLUSIONS: TiNOX coating significantly reduces neointimal hyperplasia in stainless steel stents. The antiproliferative effect was similar for both TiNOX coatings, suggesting that the electrochemical properties are more important for attenuation of neointimal proliferation than the observed differences in platelet adhesion and fibrinogen binding.

Left ventricular function before and after diltiazem in patients with coronary artery disease.

Left ventricular contraction, relaxation and diastolic mechanics were investigated before and after intravenous administration of 15 mg of diltiazem in 15 patients with coronary artery disease. High fidelity left ventricular pressure measurements were performed in all 15 patients, with simultaneous biplane cineangiography in 13. The time constant of left ventricular isovolumic pressure decay was calculated from the linear relation of left ventricular pressure and its rate of change with time (negative dP/dt). Frame by frame volume analysis through one cardiac cycle was completed to construct volume-time and pressure-volume curves before and after the administration of diltiazem. After diltiazem, left ventricular peak systolic pressure decreased from 124 to 113 mm Hg (p less than 0.001), while left ventricular end-diastolic pressure and heart rate were not altered. Maximal positive dP/dt also remained unchanged. End-diastolic volume was not changed after diltiazem, but end-systolic volume increased from 48 to 52 ml/m2 (p less than 0.025); as a result, ejection fraction decreased slightly from 57 to 55% (p less than 0.025). The time constant of left ventricular pressure decay and maximal negative dP/dt decreased from 58 to 54 ms (p less than 0.025) and from -1,404 to -1,321 mm Hg/s (p less than 0.025), respectively. Peak early diastolic filling rate increased from 621 to 752 ml/s (p less than 0.01) in association with an increase in filling volume during the first half of diastole from 60 to 68% (p less than 0.005). No consistent displacement of the diastolic pressure-volume curve was observed after diltiazem.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise-induced vasomotion of angiographically normal and stenotic coronary arteries improves after cholesterol-lowering drug therapy with bezafibrate.

OBJECTIVES: We attempted to determine whether the coronary vasomotor response to exercise improves after cholesterol-lowering drug therapy with bezafibrate. BACKGROUND: Hypercholesterolemia and other coronary risk factors are associated with impaired endothelium-dependent coronary vasomotor response to physiologic or pharmacologic stimuli, even in the absence of overt coronary atherosclerosis. It is still unknown whether the coronary artery vasomotor response to dynamic exercise improves under cholesterol-lowering drug therapy. METHODS: Of 15 male patients (age 51 +/- 7 years [mean +/- SD]) included in the study, 7 had markedly elevated cholesterol levels (> or = 6.5 mmol/liter, therapy group), and 8 had normal or slightly elevated cholesterol levels (< 6.5 mmol/liter, control group). At baseline and after 7 months of cholesterol-lowering therapy with bezafibrate (400 mg/day) in the therapy group, coronary vasomotor response to dynamic exercise (percent change in cross-sectional vascular area at maximal exercise vs. rest [100%]) in normal and stenotic, previously dilated vessels was assessed by quantitative coronary angiography. RESULTS: During follow-up, total serum cholesterol levels in the therapy group decreased from 7.8 +/- 1.1 to 5.8 +/- 1.1 mmol/liter (p = 0.0001) and did not change significantly in the control group (from 5.4 +/- 0.9 to 6.0 +/- 1.2 mmol/liter, p = NS). Exercise-induced vasomotor response (at similar work loads in the therapy and control groups) in both normal and dilated stenotic coronary arteries improved significantly in the therapy group, from 100 +/- 9% to 109 +/- 7% (p = 0.0001, cross-sectional area at rest 100%) and from 80 +/- 11% to 106 +/- 7% (p = 0.0002), respectively, but did not improve during follow-up in the control group. CONCLUSIONS: The present study indicates that cholesterol-lowering drug therapy with bezafibrate for 7 months improves exercise-induced vasomotion of angiographically normal coronary arteries. Seven months after coronary angioplasty, the reduction in serum cholesterol levels is, at least in part, associated with a restoration of the initially disturbed vasomotor response of stenotic vessel segments to exercise.

Pulsus alternans: its influence on systolic and diastolic function in aortic valve disease.

Left ventricular high fidelity pressure measurements and simultaneous biplane cineangiocardiography were performed in 12 patients with severe aortic valve disease (aortic stenosis in 10, aortic insufficiency in 1 and combined valve lesion in 1). Left ventricular contractility was estimated from maximal rate of left ventricular pressure rise (max dP/dt), peak measured velocity of contractile element shortening (Vpm) and mean circumferential fiber shortening velocity. Left ventricular relaxation was assessed in 12 patients from the time constant (T) of the decline in left ventricular pressure; this constant was calculated from a nonlinear regression analysis of pressure and time (method 1) and a linear regression analysis of pressure and negative dP/dt (method 2). Left ventricular diastolic function was evaluated in nine patients from simultaneous diastolic pressure-volume relations during the strong and weak beats. During pulsus alternans, heart rate and left ventricular end-diastolic pressure remained unchanged, whereas peak systolic pressure (220 versus 204 mm Hg, p less than 0.01) and end-systolic pressure (101 versus 95 mm Hg, p less than 0.01) were significantly higher during the strong beat than during the weak beat. Max dP/dt was alternating (2,162 versus 1,964 mm Hg, p less than 0.05), whereas the peak velocity of contractile element shortening remained unchanged (1.21 versus 1.18 ML/s). Systolic shortening of the left ventricular minor axis was significantly (p less than 0.02) greater during the strong (24%) than during the weak (19%) beat, but that of the left ventricular major axis remained essentially unchanged (8 versus 7%).(ABSTRACT TRUNCATED AT 250 WORDS)

Age dependency of left ventricular diastolic function in pressure overload hypertrophy.

OBJECTIVES: We sought to evaluate whether age is a determinant of left ventricular (LV) pressure overload hypertrophy and whether diastolic function influenced the aging process. BACKGROUND: The adaptation of the left ventricle to chronic pressure overload is a complex process of hormonal, structural and hemodynamic factors. Different responses in the elderly patients have been described. METHODS: LV biplane cineangiography, micromanometry and endomyocardial biopsies were carried out in 57 patients with pure or predominant aortic stenosis. Patients were classified into a senior (< 60 years, mean age +/- SD 46 +/- 10 years, n = 35) and an elderly (< 65 years; mean age 70 +/- 4 years, n = 22) study group. LV systolic function was evaluated from biplane ejection fraction and midwall fractional shortening, whereas diastolic function was assessed from the time constant of LV pressure decay, peak filling rate and the constant of myocardial stiffness. Biopsy samples were examined morphometrically for interstitial fibrosis, fibrous content, muscle fiber diameter and volume fraction of myofibrils. RESULTS: Gender distribution and the severity of aortic stenosis were comparable in the two patient groups. LV peak systolic and end-diastolic pressures were significantly higher in the elderly than in the senior group. LV ejection fraction and midwall fractional shortening were comparable in the two groups. The time constant of relaxation and the myocardial stiffness constant were greater in the elderly than in the senior group whereas the early peak filling rate was significantly reduced in the elderly group. Interstitial fibrosis was increased, although not significantly (p < 0.06), and fibrous content was enhanced (p < 0.001) in elderly patients with respect to the senior group. There was a linear correlation between age and myocardial stiffness (r = 0.55), p < 0.0001) and an inverse relation between age and early peak filling rate (r = 0.52, p < 0.0001). CONCLUSIONS: In the presence of a comparable degree of aortic valve stenosis, elderly patients (> 65 years) present with more severe LV hypertrophy than do senior patients (< 60 years). Therefore elderly patients have a more pronounced impairment of LV diastolic function, whereas systolic function is preserved. Thus, there is an age dependency of LV pressure overload hypertrophy that can be explained by the longer duration of pressure overload or an exhaustion of the adaptation process in the elderly.

Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 1978 through 1996.

OBJECTIVES: Published reports were reviewed to evaluate the characteristics of peripartal management and the late pregnancy outcome in women with pulmonary vascular disease (PVD). BACKGROUND: Pulmonary hypertension poses one of the highest risks for maternal mortality, but actual data on the maternal and neonatal prognosis in this group are lacking. METHODS: Reports published from 1978 through 1996 of Eisenmenger's syndrome (n = 73), primary pulmonary hypertension (PPH) (n = 27) and secondary vascular pulmonary hypertension (SVPH) (n = 25) complicating late pregnancy were included and analyzed using logistic regression analysis. RESULTS: Maternal mortality was 36% in Eisenmenger's syndrome, 30% in PPH and 56% (p < 0.08 vs. other two groups) in SVPH. Except for three prepartal deaths due to Eisenmenger's syndrome, all fatalities occurred within 35 days after delivery. Neonatal survival ranging from 87% to 89% was similar in the three groups. Previous pregnancies, timing of the diagnosis and hospital admission, operative delivery and diastolic pulmonary artery pressure were significant univariate (p < 0.05) maternal risk factors. Late diagnosis (p = 0.002, odds ratio 5.4) and late hospital admission (p = 0.01, odds ratio 1.1 per week of pregnancy) were independent predictive risk factors of maternal mortality. CONCLUSIONS: In the last two decades maternal mortality was comparable in patients with Eisenmenger's syndrome and PPH; however, it was relevantly higher in SVPH. Maternal prognosis depends on the early diagnosis of PVD, early hospital admission, individually tailored treatment during pregnancy and medical therapy and care focused on the postpartal period.

Effect of progression of left ventricular hypertrophy on coronary artery dimensions in aortic valve disease.

OBJECTIVES: The effect of progression of left ventricular hypertrophy on coronary artery dimensions was studied in patients with aortic valve disease. METHODS: Cross-sectional area of the left and right coronary arteries was determined by quantitative coronary arteriography in 12 control subjects and in 10 patients with aortic valve disease at baseline and after a follow-up period of 66 months. RESULTS: The cross-sectional area of the left coronary artery was larger in patients with aortic valve disease than in control subjects (left anterior descending artery 13 vs. 8 mm2, p < 0.001; left circumflex artery 13 vs. 6 mm2, p < 0.001). At the follow-up examination, cross-sectional area of the left coronary artery increased (left anterior descending artery 17 mm2, p < 0.01 vs. baseline; left circumflex artery 15 mm2, p < 0.01 vs. baseline). The cross-sectional area of the right coronary artery was not different in patients with aortic valve disease from that in control subjects. Left ventricular muscle mass was larger in patients with aortic valve disease both at baseline (269 g, p < 0.001) and after follow-up examination (339 g, p < 0.001) than in control subjects (136 g). The appropriateness of coronary artery size with respect to muscle mass was evaluated by normalizing cross-sectional area of the left coronary artery (left anterior descending plus left circumflex artery) per 100 g of left ventricular muscle mass (mm2/100 g). This index was 10.9 mm2/100 g in control subjects, and decreased in subjects with aortic valve disease from 10.3 mm2/100 g at baseline to 8.6 mm2/100 g at the follow-up measurement (p < 0.05 vs. control values). CONCLUSIONS: In patients with aortic valve disease, the progression of left ventricular hypertrophy is associated with an increase in left anterior descending and left circumflex coronary artery dimensions, whereas the size of the right coronary artery remains unchanged. Despite the enlargement of the left coronary artery, the cross-sectional area of the left coronary artery per 100 g of left ventricular muscle mass decreased. Hence, the increase in coronary artery size appears to be inadequate when the severity of left ventricular hypertrophy increases.