[Infectious endocarditis].
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Biomedical subjects
Publications and source records attributed to C K Naber.
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Strict blood pressure control is pivotal in the management of patients with aortic dissection (AD), but is frequently difficult to achieve. We determined antihypertensive medical therapy and levels of blood pressure (BP) control in 40 patients with chronic AD. Patient charts were reviewed for clinical variables, serial BP measurements, and antihypertensive drug therapy. Patients were divided into two groups: patients in group 1 had effective BP control (<135/80 mmHg), patients in group 2 had resistant hypertension (BP>/=135/80 mmHg despite prescription of at least three antihypertensive drugs). Overall, systolic BP (SBP) was 130+/-20 mmHg, and diastolic BP (DBP) was 72+/-13 mmHg. Patients received a median of 4 (1-6) antihypertensive drugs. beta-blockers were used in 38/40 (95%) patients. Effective BP control was achieved in 24/40 (60%) patients (group 1), while 16/40 (40%) patients had resistant hypertension (group 2) despite receiving significantly more antihypertensive drugs (5 [4-6] vs 4 [1-5], P=0.001). Mean SBP was 116+/-9 (101-132) mmHg in group 1 and 151+/-13 (137-181) mmHg in group 2 (P<0.001); there was no difference in DBP. Group 2 patients had a significantly higher body mass index and were younger than patients in group 1. In conclusion, in the majority of patients with chronic AD, effective BP control can be achieved, but usually requires the combination of multiple antihypertensive drugs. However, in a significant proportion of patients (40%), who appear to be younger and more obese, medical therapy fails to achieve effective BP control despite use of a multiple drug regimen.
Microbe-induced (infectious) endocarditis is an endovascular infection, caused mainly by bacteria, of cardiovascular structures. The major predilection site are the native heart valves, but involvement of implanted intracardiac foreign material is increasingly being seen. The mortality rate of infectious endocarditis depends on clinical factors and the causal agent, but also on the time of the establishment of the diagnosis and the initiation of appropriate treatment. In Germany, the current mortality rate ranges up to 18%. Between January 2003 and July 2004, with the aim of improving patient care and thus the outcome of this condition, a guideline commission worked out recommendations for the diagnosis, treatment and management of the disease for the use of general practitioners and hospital physicians, in particular microbiologists, infectiologists, cardiologists and cardiac surgeons. The basis for this guideline was the systematic search through the literature of the European guideline. On the 16th and 28th of June 2004, the entire guideline was formerly approved in a nominal group process.
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While the number of genetic polymorphisms associated with cardiovascular diseases rapidly increases, the functional implications of such gene alterations are often poorly understood. Moreover, findings from genetic association studies are often contradictory, which limits the common acceptance of a role of these genetic variants in human disease. One effective approach towards a better understanding of the pathophysiologic relevance of a gene variant is the description of its impact on dynamic or functional phenotypes such as coronary vasomotor responses to exogenous or endogenous stimuli. This brief review focuses on the impact of variants in genes of the renin-angiotensin system, the alpha2-adrenoceptor gene, and the G protein beta3 subunit gene on coronary vasomotor responses.
Arterial hypertension is one of the major cardiovascular risk factors in Western countries. Besides some well established, but rather rare forms of secondary hypertension, essential hypertension is the most common diagnosis. The hereditary nature of this disease has been well established in many familial studies. The quantitative contribution of genetic factors to blood pressure variance is estimated to be about 30%, however, the genetic background of essential hypertension is complex and currently not fully understood. Besides few monogenetic forms of Mendelian transmitted hypertension, current efforts are usually directed at the identification of single contributing genetic factors. This review is thought to highlight current strategies towards a better understanding of the genetic background of essential hypertension with particular respect to genetic variants of the renin-angiotensin system, of signaling pathways such as heterotrimeric G-proteins and alpha-adducin. Moreover, genetic association studies often fail to replicate findings from previous studies. This may be in part due to the polygenetic nature of the disease. Another potential reason may be the diversity of the investigated populations. The current results of genetic analyses of essential hypertension highlight, thus, the need for a more differentiated approach to the understanding of complex, polygenetic traits implementing gene-gene-, and gene-environment interactions or distinguished functional testing of thoroughly phenotyped cohorts under standardised environmental conditions.
Intracoronary brachytherapy is a novel, meanwhile established therapy. It is currently the only interventional procedure which has proven to effectively reduce the restenosis rates after intervention of long and diffuse in-stent restenosis. For this indication, brachytherapy can be regarded as the current treatment of choice. Randomized studies yield promising results for bypass interventions or interventions in small vessels or diabetic patients. These findings may encourage the decision to perform a percutaneous, transluminal intervention in such high-risk patients. In clinical practice, implantation of new stents in combination with brachytherapy procedures should be avoided as far as possible. In any case, the combined antiaggregatory therapy should be conducted sufficiently long to minimize the danger of late stent thrombosis. Under this treatment, the expected thrombosis rates ar within the range of placebo-treated patients. The length of the radiation source should be sufficient to cover the entire interventional injury length to avoid recurrent edge stenosis. De novo lesions are currently not a routine indication for intracoronary brachytherapy. Although intracoronary brachytherapy may effectively reduce restenosis rates in sufficiently irradiated de novo lesion segments, de novo lesions should be treated only within the set-up of controlled studies. The current available data with a follow-up period of up to 5 years show that intracoronary brachytherapy is also in the mid-term a safe and effective therapy for the reduction of restenosis after coronary interventions.
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The objective of this study was to assess the early safety and efficacy of the novel 6 Fr Angio-Seal device for routine clinical use after diagnostic cardiac catheterization and coronary angioplasty. In a prospective study, we used the 6 Fr Angio-Seal device in 180 consecutive patients (131 male, 49 female, mean age 60.7 years) for closure of femoral arterial puncture sites immediately after diagnostic (n = 108) or interventional (n = 72) coronary procedures independent of the coagulation status. All patients were monitored for 24 hr after the procedure and followed for 30 days. The closure device was successfully deployed in 95.4% after diagnostic catheterization versus 98.6% after coronary angioplasty (P = 0.963). Immediate hemostasis was achieved in 91.5% versus 90.1% of the patients (P = 0.993). Major complications were observed 1.9% versus 2.8% of the patients (P = 0.885). During 30-day follow-up, no late events or complications were reported. The 6 Fr Angio-Seal device is a safe and effective device that allows for immediate closure of femoral puncture sites after both diagnostic and interventional procedures with a low rate of major complications.
DIAGNOSIS OF INFECTIVE ENDOCARDITIS: Due to the complexity of the clinical diagnosis of infective endocarditis, standardized diagnostic schemes have been developed to improve the sensitivity and specificity of the diagnosis. The Von Reyn criteria, introduced in 1981 relied mainly on clinical, microbiological, and histopathological criteria and were for more than 10 years regarded as the diagnostic goldstandard. However, the Von Reyn criteria have a sensitivity of merely about 30-60% and their reliability is especially low in case of negative blood cultures. ROLE OF ECHOCARDIOGRAPHY: An important step towards an improved sensitivity and specificity in the diagnosis of infective endocarditis was the introduction of transesophageal echocardiography, which is far more sensitive and specific in this indication than the transthoracic approach. Besides the early detection of vegetations and complications such as abscess formation, valvular destructions or perforations, echocardiography may be helpful to identify patients at risk for a prolonged healing, embolization, or may be also used to monitor the therapeutic progress. THE DUKE CRITERIA: Implementation of echocardiography into the Duke criteria, introduced in 1994, yielded as expected, a significant higher sensitivity of up to 100% than the von Reyn criteria with an almost identical specificity. Thus, the latter were completely replaced by the Duke criteria in clinical practice. MODIFICATIONS OF THE DUKE CRITERIA: Nevertheless, some uncertainty remains, especially in culture-negative endocarditis which has led to certain modifications of the Duke criteria. Besides the implementation of unspecific inflammatory parameters such as the C-reactive protein, a positive Q-fever serology has been added and any S. aureus bacteremia is now judged as major criterion. Although a prospective evaluation has to be awaited, these modifications appear promising and should be implemented into clinical practice. CONCLUSIONS: The Duke criteria are currently the most sensitive tool in the diagnosis of infective endocarditis. It can be expected that they will help to significantly shorten the time to diagnosis, and may, thus, improve the clinical outcome.
Intracoronary irradiation is currently the most promising approach to reduce restenosis after percutaneous transluminal coronary angioplasty. Meanwhile numerous data are available concerning efficacy and safety of this novel method. These data confirm the results of preclinical studies that reported a dramatic reduction of neo-intima proliferation and negative remodeling. However, the number of reports on an elevated incidence of late stent thrombosis (> 30 days post intervention) are increasing. It is commonly suggested that the delayed neo-intima formation within vascular stents is responsible for this new phenomenon. We report the case of a 48-year-old man who underwent coronary irradiation therapy after stent placement in a de-novo/restenotic lesion. Despite an explicit recommendation of a combined anti-aggregatory therapy consisting of ticlopidine and acetysalicylic acid for at least 6 months, ticlopidine was withdrawn after 4 weeks. Two weeks later, the patient was readmitted to an external hospital with an acute myocardial infarction and successfully treated with thrombolysis. The angiographic and intravascular control, which was conducted after another two weeks, showed absolutely no neointima formation within the implanted stent. Thus, a late thrombotic occlusion of the implanted stent appears most likely to be the cause underlying the myocardial infarction. This case underlines, together with other existing reports, the importance of a prolonged, combined anti-aggregatory therapy after stent placement and subsequent intracoronary irradiation.
Gatifloxacin (GTX), a new fluoroquinolone with extended antibacterial activity, is an interesting candidate for the treatment of chronic bacterial prostatitis (CBP). Besides the antibacterial spectrum, the concentrations in the target tissues and fluids are crucial for the treatment of CBP. Thus, it was of interest to investigate its penetration into prostatic and seminal fluid. GTX concentrations in plasma, urine, ejaculate, prostatic and seminal fluid, and sperm cells were determined by a high-performance liquid chromatography method after oral intake of a single 400-mg dose in 10 male Caucasian volunteers in the fasting state. Simultaneous application of the renal contrast agent iohexol was used to estimate the maximal possible contamination of ejaculate and prostatic and seminal fluid by urine. GTX was well tolerated. The means (standard deviations) for the following parameters were as indicated: time to maximum concentration of drug in serum, 1.66 (0. 91) h; maximum concentration of drug in serum, 2.90 (0.39) microg/ml; area under the concentration-time curve from 0 to 24 h, 25.65 microg. h/ml; and half life, 7.2 (0.90) h. Within 12 h about 50% of the drug was excreted unchanged into the urine. The mean renal clearance was 169 ml/min. The gatifloxacin concentrations in ejaculate, seminal fluid, and prostatic fluid were in the range of the corresponding plasma concentrations which were 1.92 (0.27) microg/ml at approximately the same time point (4 h after drug intake). The concentrations in sperm cells (0.195, 0.076, and 0.011 microg/ml) could be determined in three subjects. The good penetration into prostatic and seminal fluid, the good tolerance, and the previously reported broad antibacterial spectrum suggest that GTX may be a good alternative for the treatment of chronic bacterial prostatitis. Clinical studies should be performed to confirm this assumption.
In a randomized crossover study, 16 volunteers (8 men, 8 women) received single oral doses of 320 mg of gemifloxacin and 400 mg of ofloxacin on two separate occasions in the fasting state to assess the urinary excretion and urinary bactericidal titers (UBTs) at intervals for up to 144 h. Ofloxacin showed higher concentrations in urine compared with those of gemifloxacin. The median (range) cumulative excretion of gemifloxacin was 29.7% (8.4 to 48.7%) of the parent drug administered, and median (range) cumulative excretion of ofloxacin was 84.3% (46.5 to 95.2%) of the parent drug administered. The UBTs, i.e., the highest twofold dilutions (with antibiotic-free urine as the diluent) of urine that were still bactericidal, were determined for a reference strain and nine uropathogens for which the MICs of gemifloxacin and ofloxacin were as follows: Escherichia coli ATCC 25922, 0.016 and 0.06 microg/ml, respectively; Klebsiella pneumoniae, 0.03 and 0.06 microg/ml, respectively; Proteus mirabilis, 0.125 and 0.125 microg/ml, respectively; Escherichia coli, 0.06 and 0.5 microg/ml, respectively; Pseudomonas aeruginosa, 1 and 4 microg/ml, respectively; Staphylococcus aureus, 0.008 and 0.25 microg/ml, respectively; Enterococcus faecalis, 0.06 and 2 microg/ml, respectively; Staphylococcus aureus, 0.25 and 4 microg/ml, respectively; Enterococcus faecalis, 0.5 and 32 microg/ml, respectively; and Staphylococcus aureus, 2 and 32 microg/ml, respectively. Generally, the UBTs for gram-positive uropathogens were higher for gemifloxacin than for ofloxacin and the UBTs for gram-negative uropathogens were higher for ofloxacin than for gemifloxacin. According to the UBTs, ofloxacin-resistant uropathogens (MICs, >or=4 mg/liter) should also be considered gemifloxacin resistant. Although clinical trials have shown that gemifloxacin is effective for the treatment of uncomplicated urinary tract infections, whether an oral dosage of 320 mg of gemifloxacin once daily is also adequate for the treatment of complicated urinary tract infections has yet to be confirmed.
The 894T allele of a G894T polymorphism in the endothelial nitric oxide synthase (eNOS) gene is associated with decreased eNOS activity, cleavage of the protein, and endothelial dysfunction. The present study evaluated the association with coronary blood flow (CBF) at rest and during adenosine (ADO)-induced hyperemia. CBF was determined by Doppler flow wire and angiography in 97 left anterior descending arteries of individuals without coronary artery disease. At rest, average peak velocity (APV) was lower and coronary vascular resistance (CVR) was higher in homozygous carriers of the 894T allele than in heterozygotes and individuals without the 894T allele. CBF tended to be lower in eNOS 894T allele carriers. During ADO-induced hyperemia (18 microg ic), APV, CVR, and CBF were not statistically different between the genotypes. The reduced APV at rest in conjunction with an increased CVR indicates a vasomotor dysfunction related to an increased microvascular resting tone in eNOS 894T allele carriers.
Treatment of subclavian artery stenosis by percutaneous balloon angioplasty and adjunctive stent placement was shown to be safe and efficacious, but it may be limited in tight stenoses and long occlusions. We describe the case of a patient who experienced progressive angina pectoris associated with signs of cerebrovertebral insufficiency 9 yr after bypass surgery, including left internal mammary artery (LIMA) grafting to the left anterior descending coronary artery. Angiography showed reversed flow through the LIMA graft into the subclavian artery and a 4-cm occlusion beginning at the origin of the left subclavian artery, representing a rare coronary-subclavian steal syndrome. After a conventional approach failed, recanalization was performed successfully using laser guide wire angioplasty with adjunctive stent placement in a combined radial and femoral approach.
Calcium antagonists are used in interventional cardiology to prevent coronary vasoconstriction or to overcome the no-reflow phenomenon. The aim of the current study was to evaluate the dose-dependent effects of intracoronary verapamil on systemic and coronary hemodynamics. In 20 patients scheduled for routine coronary angiography, heart rate, blood pressure, and ECG recordings were recorded continuously and intracoronary flow velocity was obtained by intracoronary Doppler measurements in angiographically normal vessels. The cross-sectional area, measured by quantitative coronary angiography, allowed the calculation of coronary blood flow (CBF) and the coronary vascular resistance index (CVRI). Without premedication, increasing dosages of verapamil (0.01 mg, 0.1 mg, 1.0 mg, and 2.0 mg) were injected into the left coronary artery. Intracoronary verapamil administration led to a decrease in systemic blood pressure only after administration of 1.0 mg or 2.0 mg (change in mean arterial pressure: from 87.6 +/-14.6 mmHg to 80.1 +/- 14.9 mmHg and 78.5 +/- 13.9 mmHg, respectively; both P < 0.05) without a change in heart rate. Epicardial diameters of the left coronary artery increased only at dosages of 1.0 mg and 2.0 mg (from 2.14 +/- 0.4 mm to 2.22 +/- 0.3 mm, P < 0.01), whereas the coronary blood flow velocity increased significantly at the smallest dosage of 0.01 mg (from 19.9 +/- 8.7 cm/s to 33.2 +/- 14.9 cm/s, P < 0.001) and was further enhanced with increasing dosages. CBF increased and CVRI decreased at every dosage of verapamil compared with baseline values. CBF increased also after 0.1 mg (from 13.5 +/- 6.5 mL/min to 19.5 +/- 9.3 mL/min; P < 0.05), reaching a maximal effect after administration of 1.0 mg verapamil (26.3 +/- 16.1 mL/min, P < 0.05). Application of 2.0 mg did not further increase CBF compared with 1.0 mg. Intracoronary application of verapamil leads to a decrease in systemic blood pressure at higher dosages, whereas heart rate remains unchanged at any dosage. The maximal increase in coronary blood flow and decrease in vascular resistance can be reached by administration of 1.0 mg verapamil into the left coronary artery.