Biomedical subjects

M Wiemer

Publications and source records attributed to M Wiemer.

10 recordsLinked to original sources

PubMed2001

Stroke is not a contraindication for urgent valve replacement in acute infective endocarditis.

BACKGROUND AND AIM OF THE STUDY: A treatment dilemma arises when endocarditis is complicated by cerebral embolism. Secondary cerebral hemorrhagic complications may arise following suppression of coagulation during extracorporeal circulation. Extensive valvular vegetation is regarded as an indicator for urgent surgery. The study aim was to determine the relative risk of thromboembolic complications, and to analyze the prognostic influence of different treatment strategies following onset of these complications, in particular, secondary cerebral hemorrhagic events after urgent surgery. METHODS: Between 1978 and 1993, endocarditis was diagnosed in 288 consecutive patients. Patients treated before 1982 (6.9%) were analyzed retrospectively. The remaining patients (93.1%) were followed prospectively (mean 4.3+/-1.7 years). RESULTS: In 50 patients (17.4%), the clinical course was complicated by one embolism, and in 58 patients (20.2%) by recurrent embolisms. In total, 71% of all embolisms were cerebral events. The operated patients were categorized with regard to the time between recurrent thromboembolic events and cardiac surgery (<72 h, 3-8 days, and >8 days). The prognosis for patients operated within 72 h was significantly more favorable (p <0.0001) than for those treated medically. Patients undergoing cardiac surgery more than eight days after stroke, and those treated conservatively, had poor prognoses. CONCLUSION: When endocarditis is complicated by stroke, it is recommended that cardiac surgery be performed within 72 h of the cerebral embolism, when the risk of secondary cerebral hemorrhage appears to be low. Cranial computed tomography is obligatory immediately before surgery in order to identify patients with early reperfusion hemorrhages due to spontaneous fragmentation of the thrombus. In these patients, cardiac surgery must be postponed because of the high risk of severe cerebral bleeding during extensive perioperative anticoagulation, and is only justified in the case of an otherwise unfavorable prognosis.

Acute Disease↗

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

[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

Optimal Frequency of Patient Monitoring and Intensity of Oral Anticoagulation Therapy in Valvular Heart Disease.

The antithrombotic effect of oral anticoagulation therapy and the incidence of anticoagulant-related bleeding complications are both closely correlated with the intensity of treatment. The optimal intensity of oral anticoagulation for an individual patient is the target INR that results in the lowest incidence of thromboembolic plus bleeding complications. For patients with native valve lesions, one must consider the cardiac morphology and pathophysiology, for example, the etiology of the disease, left atrial diameters, loss of active atrial contraction (atrial fibrillation), left ventricular pump function, and left ventricular diameters, to determine an optimal INR target. In patients with prosthetic devices, the "thrombogenicity" of the heart valve prosthesis is an additional risk factor for intracardiac thrombus formation and thromboembolic episodes. This "thrombogenicity" may vary significantly from device to device. INR self-testing improves the overall prognosis of patients on lifelong oral anticoagulation therapy because patients remain more precisely within that target therapeutic INR range. For most patients under phenprocoumon, one to two INR measurements per week are a sufficient frequency to provide a stable intensity of anticoagulation.

Journal Article↗

PubMed1995

[Recurrent immune thrombocytopenia: a rare complication after contrast medium injection].

HISTORY AND CLINICAL FINDINGS: In a 66-year-old woman with unstable angina, treated with 20,000 IU heparin daily for 6 days, platelet count fell dramatically from 310,000 to 1000/microliters 8 hours after injection of 90 ml of contrast medium (Iopromide) during coronary angiography. In addition to a marked tendency towards spontaneous bleeding she developed a large haematoma at the site of the arterial puncture, with a fall in haemoglobin to 9 g/dl, and acute renal failure. TREATMENT AND COURSE: Red blood cell and platelet infusions were given, together with cortisone, 1000 mg, and immunoglobulins. Platelet count returned to within normal limits after 8 days. Two haemodialyses initiated polyuria, followed by rapid normalization of kidney function. No antibodies against iopromide, iopamidol, heparin or heparinoids were found. At an emergency coronary balloon angioplasty 3 weeks later iopamidol was injected (45 ml). Again there was a profound fall in platelets to 1000/microliters, associated with acute renal failure. Treatment identical to that after the first episode brought about complete normalization. CONCLUSION: The reported reactions were most likely due to immune thrombocytopenia after administration of contrast medium.

Acute Kidney Injury↗

PubMed1995

Late prosthetic valve endocarditis.

Prosthetic valve endocarditis remains an extremely serious complication, with a low but increasing incidence. 'Late' endocarditis, occurring more than 60 days after surgery, is relatively infrequently associated with staphylococci, Gram-negative bacteria and fungi so characteristic of the endocarditis that occurs earlier. A probable source of infection can be found in 25%-80% of patients, the most frequent causes being dental procedures, urological infections and interventions, and indwelling catheters. The most common organisms are S. epidermidis, S. aureus, viridans streptococci and enterococci. The general principles of antibiotic treatment are similar to those for native valve endocarditis, but antibiotic treatment needs to be more prolonged and dosages should be used which result in maximal, nontoxic concentrations. Oral anticoagulants should be stopped and replaced by intravenous heparins. Surgical reintervention is called for if there are large highly mobile vegetations in the mitral position or within 72 h if there are cerebral thrombo-embolic episodes.

Endocarditis, Bacterial↗