Biomedical subjects

A Hagendorff

Publications and source records attributed to A Hagendorff.

At least 19 recordsLinked to original sources

PubMed2005

[Quality assurance in echocardiography. Three-level system in formation and qualifying and concept of an external quality review].

Measures of quality assurance in echocardiography can be categorized according to standard principles into measures of reviewing structure, processing, and results. This document contains 1) the description of a three level system for education and qualifying in echocardiographic examinations (quality of structure) and 2) the draft of an external quality assurance process for reviewing the results of one echocardiographic investigator or of one laboratory of echocardiography (quality of results). The document also contains a draft description of a nationwide independent institution for certification, which is needed for both projects.A level 1 investigator should be able to perform and interpret a basic investigation. A basic investigation allows to exclude most of all cardiac diseases that can be diagnosed by echocardiography, and pathological findings should be filtered out. A level 2 investigator is able to perform an extended examination, and a comprehensive echocardiographic diagnosis can be established after her or his examination. Additional specific training and experience is necessary to be certified for TEE and stress echo examinations. A level 3 echocardiographer has done research work in echocardiography and should have performed certified teaching courses in echocardiography. The external quality assurance process should provide the possibility to certify the results and reports of a single investigator or of an echo laboratory, according to standard principles of reviewing the records. The process of certification is exclusively performed on a voluntary basis. The nationwide institution of certification should be part of the academy of education in cardiology of the German Society of Cardiology.

Cardiology↗

PubMed2005

Malignant oesophago-pleuro-pericardial fistula in a patient with oesophageal carcinoma.

Pericardial and cardiac fistulae secondary to oesophageal or gastric tumours are a rare complication. We report about a 50-year-old male patient with a 10-month history of distal oesophageal carcinoma with lung and liver metastases who was referred to our hospital after 6 cycles of palliative chemotherapy at the beginning of March 2004. The patient presented with dysphagia, dyspnea, tachycardia, and hypotension. Purulent pericardial and bilateral pleural effusion was diagnosed, and the patient was treated with antibiotics, repeated pleurocentesis and pericardial drainage with daily polihexanide lavage. Oesophagogastroduodenoscopy, Peritrast swallow and computed tomographic scans of chest revealed a malignant oesophago-pleuro-pericardial fistula. A total of three coated, expandable metal stents were inserted into the oesophagus, which sealed successfully the fistula. Unfortunately, the patient succumbed to his carcinoma three months later.

Esophageal Fistula↗

PubMed2005

[Echocardiographic functional analysis of patients with rheumatoid arthritis and collagen diseases].

Cardiac manifestations were observed in patients with rheumatoid arthritis and other collagenoses. Echocardiography is a method of choice to detect pathologies in morphology and function of the heart. Pathophysiologically inflammatory alterations of the endo- as well as perimyocardium can be explained in these patients. In addition, in patients with collagenoses, the coagulation system is activated and the reactivity of the endothelium is reduced. Thus, thrombus formation at the heart valves with consecutive stenosis and/or regurgitations as well as ischemia-induced regional wall motion defects due to reduced vasodilator response of the coronary arteries can be expected. In the literature in patients with rheumatoid arthritis and other collagenoses, pericardial effusion and pulmonary hypertension are most frequently described. The echocardiographic analysis, however, is more complex due to the variability of the patient cohort. Quantification of valve defects and the analysis of wall motion and perfusion at rest and during stress is necessary to detect early changes of the diseases. The prerequisites for successful diagnostic echocardiography in these patients are the knowledge of modern echocardiographic techniques like tissue Doppler and contrast echocardiography and clinical experience with patients with rheumatoid arthritis and other collagenoses. The standardization of the echocardiographic diagnostic procedure becomes more and more important for reproducibility and comparability of the results.

Arthritis, Rheumatoid↗

PubMed2004

Estimation of vasodilator response by analysis of Doppler intensity kinetics with myocardial contrast echocardiography using an intravenous standardized bolus administration.

HYPOTHESIS: Myocardial perfusion can be analyzed by the first pass of Doppler intensity (DI) signals in the myocardium by myocardial contrast echocardiography with triggered power Doppler harmonic imaging (PDHI). METHODS AND RESULTS: DI versus time plots during 1:1 triggering was acquired during a mechanically standardized intravenous bolus application of Levovist (400 mg ml(-1); 3 ml min(-1)) at rest and during vasodilator stress with dipyridamole. Data were analyzed in 21 patients (pts) with normal coronary arteries and in 6 pts with left anterior descending artery (LAD) stenosis. Transthoracic distal LAD-flow velocities could be determined in 7 normal pts. At stress the DI wash-in rate and the DI plateau increased (3.14+/-0.3 versus 5.06+/-0.4 DI s(-1); 24.6+/-2.5 versus 30.8+/-1.8 DI, respectively). To analyze the effect of heart rate on the DI versus time plots investigations were performed in 7 additional controls at rest and during rapid pacing. Heart rates below 100 bpm did not disturb the DI kinetics at 1:1 triggering. CONCLUSIONS: Myocardial perfusion can be assessed by the analysis of the first pass DI kinetics using Levovist. The estimation of vasodilator response by PDHI seems to be an alternative to the determination of coronary flow reserve.

Aged↗

PubMed2004

Myocardial contrast echocardiography demonstrates myocardial hypoperfusion in the LAD territory in patients with acute chest pain at rest--a prospective study using power Doppler harmonic imaging with intravenous bolus application.

AIMS: Using a previously published algorithm we hypothesize that myocardial contrast echocardiography (MCE) with power Doppler harmonic imaging (PDHI) is able to detect regional hypoperfusion within the territory of the left anterior descending artery (LAD) using intravenous (i.v.) injection of contrast in patients (pts) with coronary syndrome at rest. METHODS AND RESULTS: Forty-seven consecutive patients (pts) were prospectively evaluated using a standardized i.v. bolus application of OPTISON. MCE data were acquired within 2 h before angiography. Cut-off Doppler intensity (DI)-values determined in the apical, mid, and basal septum were distinguished between normal and hypoperfused myocardium (e.g. 23.5 and 22.5 dB for maximum DI of the apical or mid-septum triggering on every third heart cycle). Seventeen of 42 pts were classified as normal and the remaining 25 pts as pathologic (10 of these 25 pts had elevated troponines). Angiography detected open vessels or TIMI-III-flow in 15 pts of the normal MCE group, significant stenosis (>70%) or reduced TIMI-flow in 22 pts of the pathologic MCE group. The highest sensitivities (83-92%) were found in the apical septum. CONCLUSION: Assessment of the myocardial perfusion deficits in the LAD territory of pts with acute coronary syndrome is feasible with MCE with PDHI using an i.v. bolus protocol.

Acute Disease↗

PubMed2003

Chronic regulation of the expression of the gap junction protein connexin 43 in transfected HeLa cells.

Gap junction channels are essential for intercellular communication. Among the most abundant gap junction channel proteins is connexin 43 (Cx43). The goal of our study was to find out, whether Cx43 content may be regulated via adenylyl cyclase (AC)/cAMP/protein kinase A (PKA), protein kinase C (PKC) pathways or by a tyrosine kinase coupled pathway, i.e. TNF alpha-receptor dependent pathway. Therefore, we used HeLa cells transfected with Cx43 and exposed these cells for 24 h to either db-cAMP (10(-4)M), forskolin (10(-5)M), the phorbolester phorbol-12,13-didecanoate PDD (10(-7)M) (or its inactive form 4 alpha-PDD), TNF alpha (10 U/ml) with or without additional treatment with the MAP kinase inhibitors SB203580 (10(-5) M, p38 MAP-kinase inhibitor) or the MEK1-inhibitor PD98059 (10(-5)M). Cx43 content was analysed using Western blot analysis. All results were confirmed by a second series of identical experiments using Cx43 immunohistochemistry. We found significantly enhanced Cx43 content in cells treated with db-cAMP, forskolin, PDD or TNF alpha (p<0.05), while 4 alpha-PDD or the solvent DMSO exerted no effect. These increases in Cx43 content could be completely suppressed by SB203580 (p<0.05) but not by PD98059. In absence of a stimulating drug, these inhibitors (SB203580 or PD98059) did not affect Cx43 content. Additional PCR experiments revealed increases in Cx43-mRNA under the influence of db-cAMP, forskolin, PDD or TNFalpha (p<0.05), which all could be completely suppressed by SB203580. From these results we conclude that 1.Cx43 content can be regulated via AC/cAMP/PKA, PKC and TNF alpha-receptor-dependent pathways 2. Activation of p38 MAP kinase is a common pathway for regulation of Cx43 content in HeLa cells

Adenylyl Cyclases↗

PubMed2003

Myocardial contrast echocardiography for assessment of myocardial perfusion at rest in a patient with left main coronary artery stenosis.

The present case will focus on the potential of hypoperfusion detection with myocardial contrast echocardiography (MCE) using power Doppler harmonic imaging (PDHI). PDHI is normally performed in a triggered mode. Microbubbles were destroyed by the ultrasound energy in the myocardium, and myocardium has to be refilled with microbubbles within the time interval between the ultrasound pulses to obtain repetitive information about perfusion. Using the contrast agent Levovist, however, real-time PDHI also results in myocardial opacification presumably due to perfusion signals of the arteriolar microbubble passage. A 45-year-old woman with typical stress-induced angina was admitted to our department for cardiac catheterization. Prior to the angiography a conventional echocardiogram showed normal left ventricular function. Tissue Doppler, however, demonstrated postsystolic longitudinal shortening of the septal, anterior, and lateral wall regions. Myocardial contrast echocardiography with triggered PDHI showed complete opacification of the myocardium at rest. Using real-time PDHI with Levovist, the septum could not be opacified. The consecutive angiography documented a severe unprotected main coronary artery stenosis. After angioplasty and stent implantation, MCE measurements were repeated. Repetitive intravenous bolus injections of Optison during triggered PDHI showed no differences to the investigation prior to the angioplasty. Using real-time PDHI with Levovist, however, there was a marked difference in comparison to the pre-interventional analysis. A complete opacification of the apical septum was observed. The present case suggests that different MCE techniques can analyze different compartments of the myocardial vasculature in clinical practice. This methodological comparison between triggered and real-time PDHI shows obviously differences in the DI signal detection due to the different microbubble behavior. Clinicians should be aware of the potentials of MCE to improve noninvasive diagnostic procedures in patients with ischemic heart disease.

Albumins↗

PubMed2003

Assessment of regional myocardial hypoperfusion with myocardial contrast echocardiography using intravenous bolus application in patients with acute chest pain: a double case report.

Myocardial contrast echocardiography using power Doppler harmonic imaging is able to document myocardial hypoperfusion. Two case reports demonstrate the potential of intravenous bolus application of microbubbles in patients with acute chest pain due to myocardial ischaemia to detect regional low flow conditions. The case reports will focus on the necessity to present Doppler intensity kinetics by Doppler intensity vs time plots or coloured M-modes to present the data more objectively. In addition, the hypoperfusion detected with myocardial contrast echocardiography via bolus injection of microbubbles can only be proven by changes of regional perfusion between repetitive myocardial contrast echocardiography measurements or by additional perfusion analysis, e.g. by scintiscanning.

Acute Disease↗

PubMed2003

Intravenous myocardial contrast echocardiography during angioplasty.

Myocardial contrast echocardiography (MCE) using power Doppler harmonic imaging (PDHI) has been reported to document regional myocardial perfusion. Two case reports demonstrate the potential of intravenous myocardial contrast echocardiography during angioplasty.

Angioplasty, Balloon↗

PubMed2002

[A hemodynamically active type II atrial septal defect in a 78-year-old patient. Indications for interventional catheter occlusion?].

HISTORY AND ADMISSION FINDINGS: A 78-year-old woman presented with a first episode of syncope. She reported increasing fatigue and dyspnoea upon exertion over a period of 20 years and chest pain 2 months prior to admission. Auscultation revealed fixed doubling of the second heart sound. INVESTIGATIONS: Laboratory tests showed increased troponin I. Transaminases were moderately elevated. Chest X-ray showed an enlarged right heart and a dilated pulmonary artery (2 cm). Echocardiography discovered a large secundum atrial septal defect with a diameter of 3 cm but no right to left shunt (no Eisenmenger reaction). Cardiac catheterization revealed a stenosis of the right coronary artery and severe systolic pulmonary hypertension of 80 mmHg. DIAGNOSIS, TREATMENT AND COURSE: A significant stenosis of the right coronary artery was successfully dilated. The ASD was closed by interventional implantation of a commercial closure device (Amplatzer). One month later, echocardiography indicated in an estimated systolic pulmonary pressure of 30 mmHg. The patient's condition improved considerably. CONCLUSION: This case is remarkable in that a very large ASD was asymptomatic up into old age and without the development of an Eisenmenger reaction. Also, large ASD can be by catheterization with the appropriate closure device. Fixed pulmonary hypertension is not obligatory. Non-invasive closure is a good alternative of surgery in elderly patients with risk factors.

Aged↗

PubMed2001

[Electrophysiological characterization of connexin 40 deficient hearts--in vivo studies in mice].

Intercellular communication is not only mediated by extracellular transmitters, but also directly by gap junction channels. One channel is composed of two hexameric hemichannels which consist of six polypeptide subunits called connexines (Cx). In the mammalian heart the following connexines have been documented: Cx37, Cx40, Cx43, Cx45, Cx46, Cx50 and Cx57. The labeling by number represents the rounded, molecular mass of the amino acid sequences given in kD. If identical connexin-isotypes form both connexons of a gap junction channel, homotypic coupling exists and a homomeric gap junction channel is formed. Different connexin-isotypes within both connexons cause form heterotypic coupling and heteromeric gap junction channels. Each channel type has specific properties regarding permeability and electrical conductance. Beside a typical age-dependent alignment of gap junction channels on the surface of the cardiac myocytes, regional distribution of the different connexins is different at distinct parts of the mouse heart. Cx40 is not found in the ventricular working myocardium of mice. In the atria as well as in the conduction system, Cx40 is the most frequently expressed. In line with the localization and the conduction properties of distinct homotypic gap junction channels, the Cx40 deficient mouse is suitable for analysis of atrial arrhythmias. Cx40-deficiency in the mouse heart results in characteristic ECG changes like first degree atrioventricular block and prolongation of the QRS duration. Thus, an impairment of the sinuatrial, intraatrial and atrioventricular conduction properties is documented in Cx40 deficient mice. These observations are associated with an increased atrial vulnerability. The Cx40 deficient mouse provides a good example of the relevance of transgenic mouse models to clarify the mechanisms of arrhythmogenesis. The clinical impact of future transgenic mouse models depends on the cooperation of geneticists, basic researchers and clinicians.

Animals↗

PubMed2001

[Is brain blood supply affected by changes in cardiac volume? Measurements of brain blood supply in healthy subjects during volume overload and in patients with artificial pacemaker by changing the pacing rate].

A constant cerebral blood flow (CBF) in the presence of systemic blood pressure changes and cardiac output (CO) alterations during physiological conditions are postulated by the mechanism of cerebral autoregulation. The aim of the present study is the analysis of CBF in pacemaker (PM) patients with unspecific neurological symptoms. CBF was measured in 9 controls and 23 pacemaker patients with 133xenon, CO using Doppler echocardiography or impedance cardiography. Mean and individual CBF in controls remained unchanged when a CO increase of 28% induced by volume overload was observed. In PM patients a mean CO increase of 38% induced by an increase of basic pacing rate caused different effects of CBF. CBF increased or decreased by about 10% or remained constant. In summary, the data suggest an impairment of cerebrovascular function in those patients with concomittant CBF changes due to CO alterations (15/23 approximately equal to 65%). Thus, the analysis of brain perfusion in PM patients with unspecific neurological symptoms is possibly a new diagnostic feature in the future. It can be discussed whether or not indication and optimizing of pacemaker therapy has to be additionally analyzed by determination of endorgan perfusion.

Adult↗

PubMed2001

Case report: regional cerebral hypoperfusion induced by ventricular tachycardia - short-term hippocampal hypoperfusion and its potential relationship to selective neuronal damage.

BACKGROUND: Focussing on regional cerebral hypoperfusion during hemodynamically stable, but borderline hypotensive, sustained ventricular tachycardia (VT) experimental studies show (1) a reduction of cerebral blood flow (CBF) during tachyarrhythmias in contrast to the concept of CBF autoregulation, (2) a mediation of hypoperfusion by neuronal and humoral mechanisms, and (3) an involvment of microcirculation due to an ischemic stress response of the cerebral tissue. The clinical relevance of these observations remains still unclear. CASE REPORTS: Two patients with coronary artery disease, left ventricular dysfunction and sustained monomorphic VT underwent electrophysiological study. VT was induced and the tracer (99m)Tc-HMPAO was injected after 3 minutes of ongoing VT. Regional CBF during this life threatening arrhythmia was determined with brain SPECT. A scanning protocol was performed after termination of VT. The measurements were repeated at baseline during normofrequent sinus rhythm (SR) one week later. CBF during SR was significantly reduced in the temporal lobe in comparison to the conditions during stable VT, particularly in the left hippocampus. CONCLUSION: The reduction of hippocampal CBF due to cerebrovascular vasoconstriction and neuronal reflex mechanism previously observed in experiments during stable, sustained VT can be confirmed in a clinical scenario by high resolution (99m)Tc-HMPAO brain SPECT. This supports the hypothesis that repetitive stable VT can play a role in the pathophysiology of cerebrovascular insufficiency. Further clinical studies are needed to analyze the impact of tachyarrhythmias on cognitive and mnemic function.

Aged↗

PubMed2000

Unique and shared functions of different connexins in mice.

BACKGROUND: Connexins are the protein subunits of intercellular gap junction channels. In mammals, they are encoded by a family of at least 15 genes, which show cell-type-specific but overlapping patterns of expression. Mice lacking connexin43 (Cx43) die postnatally from obstruction of the right ventricular outflow tract of the heart. To discriminate between the unique and shared functions of Cx43, Cx40 and Cx32, we generated two 'knock-in' mouse lines, Cx43KI32 and Cx43KI40, in which the coding region of the Cx43 gene was replaced, respectively, by the coding regions of Cx32 or Cx40. RESULTS: Heterozygous mutants were fertile and co-expressed the wild-type and the corresponding recombinant allele in all tissues analyzed. Heterozygous Cx43KI32, but not Cx43KI40, mutant mothers were unable to nourish their pups to weaning age, possibly reflecting a defect in milk ejection. Homozygous mutant males were sterile because of extensive germ-cell deficiency. The ovaries of homozygous Cx43KI32 neonates exhibited all stages of follicular development and ovulation. The hearts of homozygous Cx43KI32 neonates showed mild morphological defects, but the cardiac morphology of homozygous Cx43KI40 neonates was relatively normal. Spontaneous ventricular arrhythmias were observed in most Cx43KI40 and some Cx43KI32 mutant mice, suggesting increased ventricular vulnerability in these mice. CONCLUSIONS: The postnatal lethality of Cx43-deficient mice was rescued in Cx43KI32 or Cx43KI40 mice, indicating that Cx43, Cx40 and Cx32 share at least some vital functions. On the other hand, Cx43KI32 and Cx43KI40 mice differed functionally and morphologically from each other and from wild-type mice. Thus, these connexins also have unique functions.

Animals↗

PubMed2000

Abnormal cardiac conduction and morphogenesis in connexin40 and connexin43 double-deficient mice.

Connexin40-deficient (Cx40(-/-)/Cx43(+/+)) and connexin43-heterozygous knockout mice (Cx40(+/+)/Cx43(+/-)) are viable but show cardiac conduction abnormalities. The ECGs of adult double heterozygous animals (Cx40(+/-)/Cx43(+/-)) suggest additive effects of Cx40 and Cx43 haploinsufficiency on ventricular, but not on atrial, conduction. We also observed additive effects of both connexins on cardiac morphogenesis. Approximately half of the Cx40(-/-)/Cx43(+/+) embryos died during the septation period, and an additional 16% died after birth. The majority of the latter mice had cardiac hypertrophy in conjunction with common atrioventricular junction or a ventricular septal defect. All Cx40(-/-)/Cx43(+/-) progeny exhibited cardiac malformations and died neonatally. The most frequent defect was common atrioventricular junction with abnormal atrioventricular connection, which was more severe than that seen in Cx40(-/-)/Cx43(+/+) mice. Furthermore, muscular ventricular septal defects, premature closure of the ductus arteriosus, and subcutaneous edema were noticed in these embryos. Cx40(+/-)/Cx43(-/-) embryos showed the same phenotype (ie, obstructed right ventricular outflow tract) as reported for Cx40(+/+)/Cx43(-/-) mice. These findings demonstrate that Cx43 haploinsufficiency aggravates the abnormalities observed in the Cx40(-/-) phenotype, whereas Cx40 haploinsufficiency does not worsen the Cx43(-/-) phenotype. We conclude that the gap-junctional proteins Cx40 and Cx43 contribute to morphogenesis of the heart in an isotype-specific manner.

Animals↗

PubMed2000

[Alcohol concentration in the coronary sinus after transarterial ablation of septal hypertrophy in hypertrophic obstructive cardiomyopathy].

BACKGROUND AND OBJECTIVE: The size of the resulting myocardial necrosis varies after percutaneous transarterial ablation (PTA) of hypertrophied septum in patients with hypertrophic obstructive cardiomyopathy (HOCM). It was the aim of this study to discover whether the alcohol concentration in coronary sinus (CS) blood is a useful and appropriate parameter and what conclusions can be drawn from it. PATIENTS AND METHODS: PTA was done in four patients (two women and two men, aged 30-53 years) with HOCM. Before the intervention the gradient across the left ventricular outflow tract ranged form 20 to 80 mmHg, postextrasystolic it ranged from 40 to 180 mmHg. 1 x 2 ml ethanol was injected into the first septal branch in 3 patients, 2 x 2 ml in one. The alcohol concentration in coronary sinus blood was measured every 30 sec for up to 5 min before and after ablation. The amounts were compared with the size of the akinetic area in the echocardiogram and the maximal value of creatine kinase, as a measure of the size of myocardial necrosis. RESULTS: The left ventricular outflow gradient was reduced in all patients, to 0-30 mmHg and postextrasystolic to 30-90 mmHg. A pacemaker had to be implanted in one patient who developed a 3 degrees AV block. The alcohol concentration in coronary sinus blood ranged from maximally 1.53 and 0.23 per thousand after 30 sec and then fell to 0.56-0.12 per thousand after 5 min. The patient with the highest CS alcohol concentration also had the highest maximal value for creatine kinase (68 mumol/l) and the largest akinetic area in the echocardiogram. CONCLUSION: The extent of myocardial necrosis can probably be estimated from the CS blood concentration of alcohol after alcohol ablation. If, after the first injection, high alcohol concentrations are measured, further alcohol injections are not indicated.

Adult↗

PubMed2000

[Cardiac pacemaker therapy for optimizing brain circulation. A possible prevention for cerebrovascular diseases?].

HISTORY AND CLINICAL FINDINGS: A 78-year-old patient experienced dizziness, impairment of mnemic and cognitive function, chronic fatigue and recurrent syncope. INVESTIGATIONS: Hypertensive heart disease, reduced left ventricular function, and ventricular ectopia classification Lown IVb was documented. Computed tomography showed minimal brain atrophia. Stenoses of the brain supplying arteries and of other intracranial diseases were excluded. A distinct correlation between cardiac output and cerebral blood flow in correspondence to changes of heart rate were found (cardiac output 4.2 l/min during sinus rhythm, 7.4 l/min during temporary atrial pacing--AAI-Mode with a pacing rate of 90/min; 4.8 l/min--AAI-Mode with a pacing rate of 120/min; cerebral blood flow: 70, 74 and 62 ml/100 g per minute, respectively). Thus, impairment of cerebral blood flow autoregulation can be assumed. TREATMENT AND COURSE: After implantation of a permanent pacemaker the patient was without any complaints. The mnemic and cognitive function improved, dizziness and fatigue disappeared. Synopsis did not occur. 14 months later a sudden onset of complaints occurred caused by atrial fibrillation (heart rate 120/min). Cardiac output and cerebral blood flow were now 4.0 l/min and 35 ml/100 g per minute. After antiarrhythmic drug therapy and restoration of sinus rhythm cardiac output and cerebral blood flow increased and the complaints disappeared again. CONCLUSION: In patients with impaired capacity of cerebral autoregulation a reduced cardiac function and output can induce a reduction of cerebral blood flow. Thus, impairment of mnemic and cognitive function as well as other unspecific neurological deficits can be caused. In these cases pacemaker therapy has to be discussed as an effective therapeutical concept.

Aged↗

PubMed2000

[Fractional flow reserve as a deciding criterion for intervention in patients with 50% coronary stenoses and impaired myocardial perfusion].

BACKGROUND: A fractional flow reserve (FFRmyo) < 0.75 is a well validated parameter for significance of coronary stenoses in cases of normal myocardial function. We used the FFRmyo limit in patients with impaired myocardial perfusion by myocardial infarction and/or hypertension for intermediate stenoses of the LAD for decision to PTCA and checked the indication by clinical follow-up. METHODS: In 20 pts (5 women) with chest pain and visual 50 D% LAD stenoses, the FFRmyo was obtained by using a RADI-Pressure-Wire, the CFR by a densitometric technique (HODGSON), and the geometry of stenosis (minimal lumen diameter and diameter stenosis) by quantitative coronary angiography (QCA). EF and the kinetics of the anterolateral wall (expressed as radial shortening fraction) were measured by laevography. RESULTS: The mean age of our 20 pts. was 59.4 years: 13 of the pts. (65%) had a history of hypertension, 9 (45%) pts. a history of myocardial infarction. The mean diameter stenosis was 50.8%. The mean value of CFR was 2.9. The FFRmyo ranged from 0.66 to 0.90, the mean value was 0.78. The 12 pts. with FFRmyo > or = 0.75 (60%, group A) were treated with the usual anti-anginal medications. A PTCA was performed only in patients with FFRmyo < 0.75 (N = 8 (40%), group B). Except for one pt. with instent restenosis, in the 7 pts. with denovo stenoses stent implantation was performed. Significant differences between the groups A and B were seen only for the total number of myocardial infarctions (8/12 vs. 1/8) and diameter stenosis (48.5% vs. 54.3%). All lesions of group B had a diameter stenosis of 50% or higher. CFR correlated significantly with the radial shortening fraction (r = 0.75), minimal lumen diameter (r = -0.51) and diameter stenosis (r = -0.46). FFRmyo correlated with diameter stenosis (r = -0.47) only. All pts. treated with PTCA were primarily free of pain or reduced angina at least 1 CCS stage; only one developed an angina due to a restenosis (74 D%) 2 months after PTCA and stent implantation. The pts. of group A did not get worse, nor were they readmitted within 6 to 13 months after catheterization. CONCLUSIONS: Pts. with 50 D% stenoses, impaired myocardial perfusion and FFRmyo < 0.75 had a good long-term benefit concerning clinical and angiographic result. No pts. with FFRmyo < 0.75 had a D% lower than 50; therefore, the PTCA of intermediate stenoses without quantification must be avoided. CFR is not helpful for a decision to PTCA in such cases, because a normal value of CFR is relevant only.

Aged↗