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Biomedical subjects

D Horstkotte

Publications and source records attributed to D Horstkotte.

At least 19 recordsLinked to original sources
PubMed1999

[Acute hantavirus infection caused by a genetically newly identified viral strain. Severe and complicated course of hemorrhagic fever with renal syndrome (nephropathia epidemica)].

HISTORY AND CLINICAL FINDINGS: A 49-year-old patient, a hobby hunter, fell ill acutely with joint and limb pain, abdominal pain, nausea and subfebrile temperatures. At hospitalization, the patient was in bad general condition, showing ascites and lid edema, and acute renal failure was diagnosed. INVESTIGATIONS: Laboratory tests revealed marked thrombocytopenia (15,000/ml), leucocytosis, elevated levels of creatinine, blood urea nitrogen and liver enzymes, respectively. Blood gas analysis showed metabolic acidosis. Chest X-ray showed an interstitial fluid accumulation, abdominal ultrasound disclosed ascites and enlarged kidneys as in acute renal failure. Immunologic tests verified the diagnosis of an acute hantavirus infection, by use of specific molecular biology techniques a previously unknown virus strain was identified. TREATMENT AND COURSE: Hantavirus infections in western Europe usually show a benign course. However, in the present case, acute progressive pulmonary failure developed despite effective dialysis so that mechanical ventilation was necessary for several weeks. Dialysis had to be carried out for 17 days. As a complication a severe ulcero-destructive tracheobronchitis developed, caused by Aspergillus fumigatus. After several weeks, both renal and pulmonary function had returned to normal. CONCLUSION: Hantavirus infections may lead to severe and complicated courses also in western Europe. By use of new immunologic and molecular biology techniques a specific diagnosis is possible.

Diagnosis, Differential↗
PubMed1999

[Significance of silent myocardial ischemia for identification and optimal therapy of patients with latent coronary heart disease. Is there a marker for prognostic indication for PTCA?].

Although percutaneous transluminal coronary angioplasty (PTCA) improves the symptomatic status and exercise capacity of patients with coronary artery disease and stale or unstable angina pectoris, a beneficial effect on long-term prognosis has not been convincingly demonstrated so far. In totally asymptomatic patients with coronary artery disease, however, decision to undertake PTCA is greatly influenced by prognostic considerations. Usually, detection of silent myocardial ischemia in non-invasive examinations (exercise stress testing, ambulatory electrocardiographic monitoring) precedes the angiographic diagnosis of coronary artery disease in these patients.

Angina Pectoris↗
PubMed1999

[Non-surgical management of a perforated left anterior descending coronary artery following cardiopulmonary resuscitation].

UNLABELLED: A 49 year old male developed cardiocirculatory arrest following laparoscopic surgery of an inguinal hernia. Cardiopulmonary resuscitation (CPR) was started. The primary ECG showed ventricular fibrillation, after defibrillation a tachyarrhythmia and a newly developed right bundle branch block were documented. In addition, ST-elevations were seen in the left precordial leads. After 20 min of CPR the circulation was reestablished with high doses of catecholamines. Transthoracic echocardiography demonstrated a 7 mm pericardial effusion with mild impression of the right ventricular free wall. The patient underwent urgent heart catheterization for suspected pulmonary embolism (differential diagnosis: acute myocardial infarction). Pulmonary angiography demonstrated floating thrombi in the left main pulmonary artery, which could be fragmented using a pigtail catheter. Pulmonary angiography was followed by coronary angiography, which demonstrated a sharply interrupted left anterior descending artery (LAD), while the coronary arteries in general were found to be regular. The history, the morphology of the LAD-interruption, the concomitant pericardial effusion and the sternal and rib fractures were consistent with a type III coronary perforation in the classification of Sutton and Ellis. As contrast medium penetration into the pericardial space persisted after recanalization of the LAD, a 19 mm stent graft (Jostent) was used for closure. These grafts are constructed using a sandwich technique with an ultrathin layer of expandable polytetrafluorethylene being placed between two stents. After implantation of the stent graft no more contrast medium penetration was documented. CONCLUSION: Coronary perforations following blunt chest trauma is a rare complication, which has been described only once following CPR (2). Stent grafts can be used safely for acute closure of such perforations.

Cardiopulmonary Resuscitation↗
PubMed1998

[Precapillary pulmonary hypertension of uncertain etiology].

HISTORY AND CLINICAL FINDINGS: A 39-year-old man was hospitalized for investigation of increasing dyspnoea for 3 month. On admission he was found to have bilateral ankle oedema, an enlarged liver and loud systolic murmur over the lower sternum. INVESTIGATIONS: There were signs of right heart strain/hypertrophy on the chest radiogram and echocardiogram. After treatment of right heart failure cardiac catheterization indicated moderate precapillary pulmonary hypertension (PH) with a mean pulmonary artery pressure (PAPm) of 24 mm Hg and pulmonary vascular resistance (PVR) of 470 dyn.s.cm-5 at rest. All known causes having been excluded, the PH was classified as idiopathic. TREATMENT AND COURSE: Evidence of acute pulmonary vascular reactivity was obtained with nitric oxide (NO) inhalation and oral diltiazem, a calcium-channel blocker. The latter, at a dosage of 3 x 120 mg daily, had after 13 days achieved a persisting reduction of PVR at rest and a reduction in PAP rise during exercise. CONCLUSION: After exclusion of other causes, the acute right heart failure was found to be due to primary pulmonary hypertension. The therapeutic efficacity of diltiazem as a vasodilator can be predicted from the response to inhaled NO.

Adult↗
PubMed1998

[Emergency heart valve replacement after acute cerebral embolism during florid endocarditis].

BACKGROUND: The indication for urgent cardiac surgical interventions in patients with active infective endocarditis has to be considered carefully following thromboembolic events, because of the high recurrence rate of such complications. In the case of brain embolisms the prognostic benefit of urgent surgery has been discussed controversially as effective anticoagulation during open heart surgery may result in secondary cerebral hemorrhages. PATIENTS AND METHODS: Between 1978 and 1993 infective endocarditis (IE) was proven in 288 consecutive and prospectively followed patients (131 females, 157 males; mean age 53.6 +/- 8.7 [9 to 81] years). To analyze potential benefits and risks of an urgent surgical intervention early after embolic cerebral infarction, cumulated survival rates were calculated for patients with and without surgical intervention with special reference to incremental risk factors and the timing of surgery. RESULTS: In 50 patients (17.4%) the clinical course was complicated by one, and in 58 patients (20.2%) by recurrent embolic events. In 80% the first embolism occurred within 33 days following the first manifestation of typical signs and symptoms of IE. 80% of recurrent events were observed within 32 days following the initial embolism. 71% of all embolic events were cerebral. In patients with cerebral embolism corroborated by computed tomography (CCT), the clinical course was complicated by intracranial hemorrhage in 12.5% while it was only 1.5% for patients without cerebral embolism. Because of a lack of therapeutic alternatives, 22 of 49 patients with recurrent embolic events, of which at least one was cerebral, underwent urgent cardiac surgery within 4 to 366 hours after the first cerebral manifestation. The cumulated survival rate of patients operated within 72 hours after the initial cerebral embolism was significantly more favorable (p < or = 0.000) than for unoperated patients or those who were operated after more than 8 days. CONCLUSION: An embolic event during IE carries a more than 50% risk of recurrence. In patients with short duration of signs and symptoms of IE and postembolic echocardiographic demonstration of persistent vegetations the probability is > 80%. At least for those patients urgent surgical intervention to remove the source of infection and embolic hazard seems to be beneficial. Surgical intervention using the heart-lung-machine should be performed within 72 hours. Such early timing results in a significant lower rate of secondary cerebral hemorrhages (p < or = 0.00) than a postponed operation. To exclude early reperfusion hemorrhage due to spontaneous thrombus fragmentation, CCT should be repeated directly preoperatively.

Adolescent↗
PubMed1998

[Optimal management of primary and secondary mitral regurgitation].

While morphologic alteration of parts of the mitral valve apparatus (ventricular wall, papillary muscles, chordae tendineae, valve annulus and leaflets) may result in a loss of its functional integrity (primary mitral regurgitation, MR) mitral annulus dilatation following left ventricular enlargement or change in chamber geometry and consecutive opening of the angle between papillary muscles and valve annulus cause secondary MR. Irrespective of these etiologies MR is chronically progressive and much more than the severity of MR the grade of myocardial adaptation to the chronic volume overload is of prognostic significance. Inadequate myocardial adaptation is demonstrated by an increase of the echocardiographically determined radius (r) to wall thickness (Th) ratio (r/Th > 3.0), indicating increasing left ventricular wall stress or by an insufficient increase of the left ventricular ejection fraction (< or = 5% of resting values) under exercise conditions, e.g. with radionuclide angiocardiography (RNV). Stressecho may replace RNV in the future for this indication. Actually, stress echo is not reliable to determine changes in left ventricular ejection fraction at rest versus exercise because of systematic errors and error reproduction. There are preliminary reports on biochemical markers like noradrenaline or tumor necrosis factor alpha being helpful to determine the breakdown of myocardial adaptation mechanisms. Surgical intervention is indicated in chronic MR irrespective of the hemodynamic severity, if myocardial adaptation is inadequate. If mitral reconstruction, the surgical technique of choice, remains insufficient to restore normal valve function, mitral valve replacement with preservation of the subvalvular apparatus is unavoidable. For a deceleration of the progressive volume overload in chronic MR for which a surgical intervention is not yet indicated, a long-term afterload reducing medical therapy preferably with long acting ACE-inhibitors seem to be prognostically favorable.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

[Diagnostic approach and optimal treatment of aortic valve stenosis].

The slow progression of valvular aortic stenosis enables the left ventricular myocardium to adapt itself to the increasing afterload. When myocardial adaption is exhausted, surgical intervention is urgent, the prognosis, however, is already limited. To quantify the hemodynamic severity of aortic stenosis, transaortic pressure gradients (dp) measured by Doppler echocardiography or hemodynamically are inappropriate, because dp is significantly dependent on the transaortic flow volume. In severe aortic stenosis, despite constant narrowing of the aortic valve area, the reduced stroke volume results in decreasing transaortic pressure gradients. With aortic valve resistance or transaortic pressure loss (PL)--the quotient of pressure gradient and stroke volume--the hemodynamic severity of aortic stenosis can be described accurately. If PL is known, a decompensated aortic stenosis (PL > 1 mm Hg/ml) may be differentiated from myocardial failure of another etiology and a concomitant left ventricular outflow tract obstruction. With respect to medical therapy, the prevention of bacterial endocarditis and thromboembolic complications is important. Knowing the potential danger of syncopies and ventricular arrhythmias during exercise with increasing severity of aortic stenosis, patients have to be informed about their limited functional capacity. The occurrence of typical symptoms during the natural history of chronic aortic stenosis (e.g. dizziness, syncopes, angina pectoris, arrhythmias) manifestation of ST-T-alterations or silent myocardial ischemias and demonstration of an inadequate myocardial adaptation to the chronic pressure overload in asymptomatic patients are accepted indications for a surgical intervention. If the indication for surgery remains uncertain, stress tests (e.g. radionuclidventriculography) may be performed to demonstrate an exhausted myocardial adaptation. If the PL and the severity of aortic valve/anulus calcification is known, the progression of a chronic aortic stenosis can be estimated. This might be important, if a cardiosurgical intervention has to be performed for other indications and aortic stenosis is co-existent but does not require an intervention at that time. For prognostic reasons myocardial decompensation due to aortic stenosis is an indication for an urgent surgical intervention. Attempts for medical recompensation or bridging strategies (e.g. balloon valvotomy) worsens the prognosis significantly.

Aortic Valve Stenosis↗
PubMed1998

[Increased acceptance of the International Normalized Ratio (INR) as a monitoring parameter of oral anticoagulation therapy in Germany. GELIA Study Group].

In 1994 the German Cardiac Society recommended the International Normalized Ratio (INR) instead of "Quick's test" for the long-term management of oral anticoagulation therapy. Parallel cardiac surgical centers in Germany and Switzerland started patient recruitment for the GELIA study (German Experience with Low Intensity Anticoagulation). By the end of 1996, 862 consecutive patients with mechanical heart valve replacement had been enrolled. According to the protocol of the GELIA study, intensity of anticoagulation, methods used to control the oral anticoagulation therapy as well as other factors relevant for the anticoagulation management are reported every three months. The so far accumulated data material of the GELIA study seemed, therefore, appropriate to analyze potential changes in the acceptance of INR during the time period 1993-1996. Potential differences in the anticoagulation management were analyzed separately according to the time of enrollment of patients and changes during the follow up period, e. g., a switch from "Quick's test" to INR. Taking the time of enrollment into account, the percentage of patients who had INR-controlled oral anticoagulation therapy increased from 0% (1993), 14.3% (1994), 63.2% (1995) to 74.2% in 1996. During the follow up, there was a change from "Quick's test" to INR controls in 7 patients (1994; 2.1%), 67 patients (1995; 10.5%) and 142 patients (1996; 17.3%) with a consequent increase of INR controlled patients to a total of 34.2% in 1994, 52.0% in 1995, and 73.9% in 1996.

Administration, Oral↗
PubMed1998

[Prospective study of the incidence, pathogenesis and therapy of spontaneous, by coronary angiography diagnosed coronary artery dissection].

Spontaneous coronary artery dissection is a rare cause of ischemic heart disease. Incidence, etiology and optimal treatment are ill-defined. Between July 1995 and December 1997, we prospectively identified 42 patients (36 men, six women, mean age 59 +/- 12 years) with spontaneous coronary artery dissection among 3803 consecutive angiographic examinations in which the diagnosis of coronary artery disease was established for the first time (incidence 1.1%). In comparison to the remaining study population with stable angina pectoris (8 cases of spontaneous coronary artery dissection among 2852 patients; incidence: 0.3%), the incidence of spontaneous coronary artery dissection was significantly higher in the patient subgroups with acute myocardial infarction (13/450; 2.9%) and with unstable angina pectoris or postinfarction angina (21/501; 4.2%). Dissection was most frequently located in the left anterior descending coronary artery (19 cases), followed by the right coronary artery (15 cases) and the left circumflex coronary artery (8 cases). Because of an ambiguous angiographic lesion appearance intravascular ultrasound imaging was performed in 13 patients to confirm the diagnosis. The presumed etiology of spontaneous coronary artery dissection was atherosclerotic plaque rupture in 35 cases, heavy physical exercise in four cases and hormonal influences related to pregnancy and contraception in one case. In two cases, no obvious risk factor could be identified. Therapy consisted of intracoronary stenting in 24 patients (including ten patients with acute myocardial infarction), coronary artery bypass grafting (CABG) in 8 patients and balloon angioplasty (PTCA) in seven patients. Three patients were treated conservatively. During a mean follow-up period of 13.5 +/- 9.9 months, two patients died and 31 patients remained entirely asymptomatic, including all patients who were treated with CABG. Restenosis developed in three patients after stent implantation (restenosis rate: 12.5%). Following primary PTCA, spontaneous coronary artery dissection recurred in two patients, one of whom subsequently died.

Adult↗
PubMed1998

The impact of vessel and catheter position on the measurement accuracy in catheter-based quantitative coronary angiography.

BACKGROUND: The calculation of absolute artery dimensions in quantitative coronary angiography is usually carried out by catheter calibration. It is based on the proportional comparison of the dimension of the imaged artery segment to the dimension of the imaged angiographic catheter of known size. This calibration method presumes an identical radiographic magnification between angiographic catheter and artery segment of interest. However, due to the different intrathoracic location of both objects the radiographic magnification or calibration factor is often not identical for a given angiographic projection. The aim of this study was to quantify the magnification error (out-of-plane magnification error) for the major coronary artery segments imaged in frequently used angiographic projections. METHODS: The intrathoracic spatial location of 468 coronary segments (RCA 196, LAD 156, LCX 116) and their respective coronary catheters were established with biplane angiography and known imaging geometry data. The error in the radiographic magnification or calibration factor was then calculated for all 936 monoplane projections using the spatial coordinates and imaging geometry data. RESULTS: The mean magnitude of magnification error was 4% within all 936 measurements. The magnitude and direction of error varied with the lesion localization and the angiographic projection angle (range -12.6% to +10.6%). The error characteristics could be described with six typical error groups by stratifying the data according to the three main coronaries and two angiographic planes. In 24% of measurements, the magnification error exceeded the 5.2% error limit acceptable for reference vessel sizing. Measurements of left coronary arteries were mainly affected by it. CONCLUSION: The magnification error contributes to the calibration error in measuring arterial dimensions by quantitative angiography. This error may affect the reliability of clinical studies and the proper sizing of interventional devices. These findings could be used to improve current error correction algorithms in order to reduce the effect of the magnification error in measuring arterial dimensions.

Algorithms↗
PubMed1998

Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves.

Permanent therapy with oral anticoagulants offers the most consistent protection in patients with mechanical heart valves. Antiplatelet agents alone do not consistently protect patients with mechanical prosthetic heart valves, including patients in sinus rhythm with St. Jude valves in the aortic position. Levels of oral anticoagulants that prolong the INR to 2.0 to 3.0 appear satisfactory for patients with bileaflet mechanical valves in the aortic position, provided they are in sinus rhythm and the left atrium is not enlarged. Oral anticoagulant levels that prolong the INR to 2.5 to 3.2 are satisfactory for patients with bileaflet mechanical aortic valves and atrial fibrillation. Oral anticoagulant levels that prolong the INR to 2.5 to 3.5 are satisfactory for tilting disk valves and bileaflet prosthetic valves in the mitral position. Experience is sparse in patients with caged ball valves who had prothrombin time ratios reported in terms of INR. It has been suggested that the most advantageous INR level in patients with caged ball or caged disk valves should be as high as 4.0 to 4.9. However, others have shown a high rate of major hemorrhage with an INR that is even somewhat lower (3.0 to 4.5). The problem is self-limited, however, because few such valves are being inserted. Aspirin, in addition to oral anticoagulants, in patients with mechanical heart valves has been shown to diminish the frequency of thromboemboli. The risk of bleeding may not be increased if the INR is low. A low rate of both thromboemboli and bleeding has been shown with an INR of 2.5 to 3.5 in combination with aspirin at a dose of 100 mg/d. There are no investigations in which an aspirin dose of 81 mg/d in combination with oral anticoagulants was evaluated. Dipyripdamole may be effective in reducing the rate of thromboemboli without increasing the rate of bleeding, but data are insufficient to recommend dipyridamole over low doses of aspirin. Patients with bioprosthetic valves in the mitral position, as well as patients with bioprosthetic valves in the aortic position, may be at risk for thromboemboli during the first 3 months after surgery. Among patients during the first 3 months after surgery with bioprosthetic valves in the mitral position, oral anticoagulants administered at an INR of 2.0 to 2.3 were as effective as at an INR of 2.5 to 4.5: additionally, fewer bleeding complications were seen.

Administration, Oral↗
PubMed1998

[Intracardiac thrombosis and consecutive thromboembolisms in patients with heart valve diseases: predisposition and concepts for prevention].

For patients with acquired heart valve lesions with increased risk for intracardiac thrombosis and consequent cardiogenic embolism there is consensus that oral anticoagulation therapy improves the overall prognosis. In mitral valve lesions anticoagulation is necessary after manifestation of atrial fibrillation or in cases of unstable sinus rhythm. The risk for thromboembolic events is increasing parallel to the enlargement of the left ventricular enddiastolic diameter, the left atrial size and dropping cardiac index. Spontaneous echo contrast (so called smoke like echos) indicate a prethrombotic state. In these cases an intensive anticoagulation is indicated. Aortic valve lesions require anticoagulation after manifestation of atrial fibrillation, the first manifestation of a thromboembolism or of spontaneous echo contrast. The risk for thromboembolism is increasing parallel to the reduction of left ventricular pump function. Life long oral anticoagulation therapy should be managed by use of the International Normalized Ratio (INR), and should be individualized taking into account patient related cardiac morphology and physiology, which may predispose to cardiogenic embolism. The target INR can range between 2.0 and 4.0.

Fibrinolytic Agents↗