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Biomedical subjects

T Meinertz

Publications and source records attributed to T Meinertz.

At least 181 records · Page 10Linked to original sources
PubMed1995

Chiari's network: normal anatomic variant or risk factor for arterial embolic events?

OBJECTIVES: This study was performed to assess the prevalence of Chiari's network in patients undergoing transesophageal echocardiography and to determine whether this anomaly is associated with other cardiac lesions or is characterized by typical clinical findings. BACKGROUND: Chiari's network is a congenital remnant of the right valve of the sinus venosus. It has been found in 1.3% to 4% of autopsy studies and is believed to be of little clinical consequence. METHODS: Video recordings of 1,436 consecutive adult patients evaluated by transesophageal echocardiography over a 30-month period were reviewed for the presence of Chiari's network. Echocardiographic contrast studies had been performed in all patients with Chiari's network and were compared with those of 160 consecutive patients without a Chiari net, serving as a control group. RESULTS: Chiari's network was present in 29 of 1,436 patients (prevalence 2%). A frequently associated finding was a patent foramen ovale in 24 (83%) of the 29 patients with Chiari's network versus 44 (28%) of 160 control patients (p < 0.001). Intense right-to-left shunting occurred significantly more often in patients with Chiari's network than in control patients (16 [55%] of 29 patients vs. 19 [12%] of 160 control patients, p < 0.001). Another frequent association was an atrial septal aneurysm in 7 (24%) of 29 patients. The indication for transesophageal echocardiography was a suspected cardiac source of arterial embolism in 24 (83%) of 29 patients with a Chiari net, 13 of whom (54%) had recurrent embolic events. Chiari's network was significantly more common in patients with unexplained arterial embolism than in patients evaluated for other indications (24 [4.6%] of 522 patients vs. 5 [0.5%] of 914 patients, p < 0.001). Potential causes for arterial embolism were present in 9 of the 24 patients with a Chiari net and embolic events (atrial septal aneurysm in 7, cerebrovascular lesion in 2). In 15 (62%) of 24 patients only a patent foramen ovale could be identified. Three patients had deep venous thrombosis and pulmonary embolism at the time of arterial embolism; none had a thrombus detected within the network. CONCLUSIONS: In patients undergoing transesophageal echocardiography, the prevalence of Chiari's network was 2%, which is consistent with autopsy studies. By maintaining an embryonic right atrial flow pattern into adult life and directing the blood from the inferior vena cava preferentially toward the interatrial septum, Chiari's network may favor persistence of a patent foramen ovale and formation of an atrial septal aneurysm and facilitate paradoxic embolism.

Abnormalities, Multiple↗
PubMed1995

Simultaneous measurement of pulmonary venous flow by intravascular catheter Doppler velocimetry and transesophageal Doppler echocardiography: relation to left atrial pressure and left atrial and left ventricular function.

OBJECTIVES: The aim of our study was to compare measurements of pulmonary venous flow velocity obtained either by transesophageal Doppler echocardiography or by intravascular catheter Doppler velocimetry. Furthermore, the relation among pulmonary venous flow velocity, left atrial compliance and left atrial pressure was evaluated. BACKGROUND: Data about the relation between left atrial pressure and pulmonary venous flow velocity are controversial. METHODS: A total of 32 patients undergoing elective open heart surgery for coronary artery bypass grafting were included prospectively in the study. Pulmonary venous flow velocity (Doppler catheter) and left atrial pressure (microtip pressure transducer) were recorded simultaneously with recordings of pulmonary venous flow velocity obtained by transesophageal Doppler echocardiography. RESULTS: Agreement between Doppler catheter and Doppler echocardiographic measurements of pulmonary venous flow velocity (n = 18 patients) was analyzed using the Bland-Altmann technique. The 95% limits of agreement were -0.16 to +0.11 m/s for systolic peak velocity, -0.14 to +0.09 m/s for diastolic peak velocity and -0.12 to +0.10 m/s for atrial peak velocity. The closest agreement between both methods was found for the ratio of systolic to diastolic peak velocity, the ratio of systolic to diastolic flow duration and the time from Q deflection on the electrocardiogram to maximal flow velocity. Mean left atrial pressure was strongly correlated with the ratio of systolic to diastolic peak velocity (r = -0.829), systolic velocity-time integral (r = -0.653), time to maximal flow velocity (r = 0.844) and the ratio of systolic to diastolic flow duration (r = -0.556). The ratio of systolic to diastolic peak velocity and the time to maximal flow velocity were identified as strong independent predictors of mean left atrial pressure. Left atrial compliance was not found to be an independent predictor of mean left atrial pressure. CONCLUSIONS: Flow velocity in the left upper pulmonary vein can be reliably recorded by transesophageal pulsed wave Doppler echocardiography. Our data reveal further evidence that mean left atrial pressure can be estimated by the pattern of pulmonary venous flow velocity.

Aged↗
PubMed1995

Insulin resistance and hyperlipoproteinemia in microvascular angina: risk factors or pathogenetic link?

BACKGROUND: Patients with chest pain and normal epicardial coronary arteries (microvascular angina; syndrome X) are characterized by an impairment of myocardial perfusion reserve which may be related to functional and morphological abnormalities of the intramyocardial arterioles. METHODS: In an attempt to identify predisposing factors for microvascular angina we investigated 34 consecutive patients (15 female, 19 male; mean age 53 +/- 7 years) with microvascular angina but without hypertension or left ventricular hypertrophy. The metabolic profile, including plasma insulin, glucose, cholesterol, low-density lipoprotein cholesterol, triglycerides, very-low-density lipoprotein cholesterol and fibrinogen levels, was determined in each case. Furthermore, insulin and glucose levels were measured after an oral glucose load of 100 g over 3 h. All parameters were compared with those of a control group of 15 healthy subjects matched for age, sex and body mass index. RESULTS: The systolic blood pressure in microvascular angina was 137 +/- 17 mmHg and thus higher than that of healthy controls (124 +/- 11 mmHg); diastolic blood pressure was 85 +/- 7 compared with 78 +/- 9 mmHg in controls. Insulin level was significantly elevated in patients with microvascular angina 90 min (median: 101 versus 54 microU/ml) and 120 min (median: 88 versus 51 microU/ml) after ingestion of 100 g glucose. The fasting glucose level was 98 +/- 12 versus 87 +/- 7 mg/dl in controls. Glucose concentration was also elevated after 30 min (176 +/- 28 versus 148 +/- 32 mg/dl), after 45 min (198 +/- 35 versus 152 +/- 53 mg/dl) and after 60 min (193 +/- 44 versus 145 +/- 54 mg/dl). In microvascular angina, parameters such as total cholesterol (244 +/- 46 versus 199 +/- 29 mg/dl), low-density lipoprotein cholesterol (157 +/- 41 versus 122 +/- 18 mg/dl) and fibrinogen (377 +/- 150 versus 285 +/- 69 mg/dl) were elevated. CONCLUSIONS: The metabolic profile in patients with microvascular angina suggests a pathogenetic role of insulin resistance and hyperlipoproteinemia in the setting of impaired myocardial coronary reserve and in early stages of hypertensive heart disease.

Adult↗
PubMed1995

Programming of the pacing impulse in pacemakers connected to steroid lead systems.

The purpose of the study was to compare the feasibility of low amplitude output programming (2.5 V/0.5 msec) 3 or more months after pacemaker implantation in patients receiving steroid and nonsteroid lead systems. Chronic pacing voltage, current, and energy thresholds were determined from 0.05- to 1.0-msec pulse duration in 44 patients with steroid lead systems, and in 36 patients with nonsteroid lead systems; all patients received pacemakers from the same manufacturer, which utilized the same programming and telemetry features. Chronaxie, pulse duration at the lowest pacing current, and energy were assessed from individual threshold curves. Steroid-eluting leads had significantly lower pacing voltage, current, and energy thresholds than nonsteroid leads. A 100% safety threshold margin could be achieved in 43 (98%) patients with steroid lead systems and in 27 (75%; P < 0.05) patients with nonsteroid lead systems with output programming of 2.5 V/0.5 msec. Chronaxie (0.22 +/- 0.17 msec vs 0.44 +/- 0.31 msec; P < 0.05), pulse duration at lowest pacing current (0.28 +/- 0.12 msec vs 0.49 +/- 0.22 msec; P < 0.05), and pulse duration at lowest pacing energy (0.31 +/- 0.17 msec vs 0.53 +/- 0.22 msec; P < 0.05) were significantly shorter for steroid than for nonsteroid lead systems. In 42 patients of the former group, a 100% safety margin could be maintained either with a 2.5 V/0.3 msec or with a 1.6 V/0.5 msec output. Conclusions Low amplitude output programming can be obtained in almost all pacemakers connected to steroid-eluting lead systems, and in a significantly higher number of patients than when connected with nonsteroid leads systems.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

[Carotid sinus massage in pacemaker patients with heart rates about the pacemaker frequency].

UNLABELLED: The delivery of pacing impulses is inhibited in patients with VVI(R) pacemakers whose intrinsic heart rate is above pacing rate. Efficacy of the pacing impulse can be evaluated on surface ECG by application of a magnet on the pacemaker which temporarily induces asynchronous pacing. Carotid sinus massage can alternatively lower intrinsic heart rate below pacing rate. The study investigates in how many patients carotid sinus massage lowers heart rate below pacing rate during follow-up, and whether the efficacy is reduced in the presence of a pacing rate programmed below the nominal setting. Patients with pacing rates 61-72 ppm (group I) were compared to patients whose pacemakers were programmed to 51-60 ppm (group II) and 40-50 ppm (group III). A right- and leftsided carotid sinus massage was performed in 119 consecutive patients. Right-sided carotid sinus massage was positive in 64 and left-sided in 53 patients. The second, left-sided carotid sinus massage induced pacing in additional 11 patients. In general, carotid sinus massage lowered heart rate below pacing rate in 75 (70%) patients. Induction of pacing was significantly lower (p < 0.02) in group III (n = 31/57; 54%) compared to group I (n = 17/20; 85%). No differences were detected between group II (n = 27/42; 64%) and group I. CONCLUSION: Carotid sinus massage is a useful method for induction of pacing in patients whose intrinsic heart rate is above pacing rate.

Adult↗
PubMed1995

Clinical evidence for the fatal interaction of ventricular tachyarrhythmias, myocardial ischemia and sudden cardiac death.

During recent years, experimental data have collected convincing evidence for the fatal interaction of myocardial ischemia, ventricular tachyarrhythmias, and sudden cardiac death. In the clinical setting, data reporting on the daily relevance of such a fatal interaction lacked until recently. However, there is now increasing evidence from autoptic studies, from the evaluation of patients who survived one episode of sudden cardiac death, from the follow-up of these patients when treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and, most recently, from studies in patients with stable and especially unstable angina pectoris suffering from Holter-documented ischemic proarrhythmia, that acute and transient myocardial ischemia play an important role for the initiation as well as the aggravation of ventricular tachyarrhythmias and out-of-hospital sudden cardiac death. The present work is directed to summarize our clinical knowledge on this topic and to indicate that preventive strategies for myocardial ischemia are the "antiarrhythmic" of choice in patients with severe coronary artery disease and evidence for ischemic proarrhythmia.

Coronary Disease↗
PubMed1995

[Modern electrodes with and without steroid: effects on stimulation current of cardiac pacemakers].

The aim of the investigation was to test whether new leads without steroid, a meshwire tip leads (Ionyx 4180, CPI; n = 10) and a carbon tip lead (Facet ITP 13, Vitatron; n = 10), have electrical characteristics similar to a new steroid-eluting tip lead (CapSure SP 4023, Medtronic; n = 10) and their impact on the pacemaker's pacing current. Pacing thresholds, impedance, and R-wave amplitudes measured at implantation were similar for the three leads. One, 4 and 12 weeks after implantation both nonsteroid leads had significantly higher pacing thresholds at 0.1 and 0.3 ms pulse duration in comparison to the steroid lead (after 12 weeks at 0.3 ms steroid: 0.9 +/- 0.2 V, carbon: 2.1 +/- 0.5 V; meshwire: 1.5 +/- 0.5 V). This result was restricted to the carbon lead after 52 weeks. At 0.5 ms pulse duration higher pacing thresholds were obtained for the carbon lead (after 12 weeks at 0.5 ms; steroid: 0.8 V, carbon: 1.7 +/- 0.6 V; meshwire: 1.1 +/- 0.4 V). Impedance of the steroid lead was 531 +/- 61 ohms, 535 +/- 54 ohms, and 511 +/- 50 ohms, respectively, after 4, 12, and 52 weeks, whereas the carbon lead had significantly higher values with 652 +/- 84 ohms, 669 +/- 93 ohms, and 657 +/- 107 ohms, respectively. The impedance of the meshwired lead (4 weeks: 585 +/- 92 ohms; 12 weeks: 592 +/- 89 ohms; 52 weeks: 550 +/- 130 ohms) did not differ from the steroid lead.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

[Low pacing thresholds of ventricular pacemaker leads: not a marker for large R-wave amplitudes and high impedance values].

An optimal position of a ventricular pacing lead in the bottom or apex of the right ventricle is defined by low pacing thresholds and high R wave amplitudes. At similar pacing thresholds high pacing impedance additionally reduces the pacing current delivered by the pacemaker. Finding an optimal position for the pacing lead would be facilitated if locations with low pacing thresholds are usually associated with great R wave amplitudes and high pacing impedance. This study assessed the relationship between ventricular pacing thresholds, R wave amplitude, and pacing impedance for present-day pacing leads at implantation. For this purpose the acute lead performance of the unipolar lined lead "CapSure SP 4023" (Medtronic) was studied in 194 patients. PSA 5311 (Medtronic) was used to measure pacing thresholds at 0.5 ms in steps of 0.1 V and impedance at 5.0 V/0.5 ms and to register filtered R wave amplitude. Pacing thresholds were 0.4 +/- 0.2 V (range 0.1-1.2 V) and impedance 576 +/- 161 ohms (range 262-1200 ohms). An intrinsic rhythm was observed in 150 patients with an R wave amplitude of 13 +/- 5 mV (range 3-28 mV). There was no statistically significant correlation between pacing threshold and R wave amplitude (r = -0.09). In respect to impedance, neither the correlation with pacing threshold (r = 0.07) nor that with R wave amplitude (r = 0.18) was statistically significant. In conclusion, most patients had pacing thresholds < 0.5 V at 0.5 ms pulse duration and R wave amplitudes > 10 mV; fewer than 5% of the patients had pacing thresholds > 0.6 V or R wave amplitudes < 5 mV. Lead locations with low pacing thresholds are usually not associated with great R wave amplitudes or high impedance.

Adult↗
PubMed1994

Continuous monitoring of acute myocardial ischemia by the implantable cardioverter defibrillator.

The present generation of implantable cardioverter defibrillators (ICDs) provides a very effective device for monitoring and treating life-threatening ventricular tachyarrhythmia. Patients at risk of sudden cardiac death who are directed to this form of treatment usually have severe coronary artery disease, previous myocardial infarction, and low ejection fraction. Progression of the underlying heart disease predisposes these patients to subsequent ischemic events, including symptomatic and asymptomatic myocardial ischemia and reinfarction, which carry a substantial risk of fatal ventricular proarrhythmia. Multipolar lead configurations presently available in the ICD appear to be effective in assessing acute myocardial ischemia as induced by exercise testing or transient coronary artery occlusion. Continuous monitoring of myocardial ischemia (COMONI) by a sophisticated, multimodal ICD appears to be feasible, may offer the means to closely supervise progression and various complications of the underlying heart disease, and may help to guide automatic or interactive antiischemic treatment.

Algorithms↗
PubMed1994

Angiotensinergic versus nonangiotensinergic hemodynamic effects of converting enzyme inhibition in patients with chronic heart failure. Assessment by acute renin and converting enzyme inhibition.

BACKGROUND: The contribution of nonangiotensinergic effects of converting enzyme inhibitors to their hemodynamic effects in patients with chronic heart failure is not clear. A comparison of the effects of renin and converting enzyme inhibition should help to clarify this issue. METHODS AND RESULTS: Thirty-six patients with chronic heart failure (New York Heart Association class II or III) were randomly assigned to receive double-blind either intravenous placebo, the renin inhibitor remikiren, or the converting enzyme inhibitor enalaprilat followed by coinfusion of a second placebo infusion, the addition of remikiren to enalaprilat, or the addition of enalaprilat to remikiren, respectively. Systemic hemodynamics (Swan-Ganz and radial artery catheters) were measured before (rest and submaximal recumbent bicycle ergometry), during (rest), and at the end (rest and exercise) of each 45-minute single- or combination-infusion period. Placebo did not change hemodynamics or renin activity. Effective inhibition of the renin-angiotensin system by remikiren and enalaprilat was indicated by increases of plasma immunoreactive renin together with rapid and complete inhibition of renin activity after remikiren and an increase after enalaprilat (all P < or = .05). Remikiren and enalaprilat rapidly and to a similar extent reduced resting blood pressure through a reduction of systemic vascular resistance, and these changes were significantly correlated to baseline plasma renin activity. Both compounds also decreased pulmonary artery, pulmonary capillary wedge, and right atrial pressures to a similar extent (P < .05). During exercise, pulmonary capillary wedge and right atrial pressures were equally reduced and stroke volume index was increased with remikiren and enalaprilat (P < .05) for both). The combination of converting enzyme with renin inhibition or vice versa did not cause additional hemodynamic changes. CONCLUSIONS: Specific renin inhibition in patients with chronic heart failure produces short-term hemodynamic effects that are almost indistinguishable from those of converting enzyme inhibition. This finding and the lack of additional effects of converting enzyme inhibition added to renin inhibition suggest that nonangiotensinergic effects of converting enzyme inhibitors do not play a significant role in their short-term hemodynamic effects in patients with chronic heart failure.

Adult↗
PubMed1994

[Amiodarone and verapamil/quinidine in treatment of patients with chronic atrial fibrillation].

Rapid, reliable and safe reestablishment of sinus rhythm is the major aim of pharmacologic treatment in patients with chronic atrial fibrillation. The mainstay of therapy in this arrhythmia has been quinidine. More recently, amiodarone was shown in noncomparitive studies to be superior to class IA agents under certain conditions. In 40 patients with atrial fibrillation persisting for 4 weeks up to 2 years, the efficacy and safety of either quinidine and verapamil (days 1 to 3, quinidine 1,500 mg/day; days 4 to 6, quinidine 1,500 mg+verapamil 240 mg/day) or amiodarone therapy (days 1 to 3, amiodarone 1,200 mg/day intravenously; days 4 to 14, amiodarone 800 mg/day orally) were randomly examined. Responders continued on their effective medication for 3 months. Thereafter, all patients were treated with a fixed regimen of quinidine (480 mg/day) plus verapamil (240 mg/day) for up to 2 years. During atrial fibrillation, quinidine reduced mean ventricular cycle length by 40 ms (-5%), quinidine and verapamil increased mean cycle length by 57 ms (8%) and amiodarone by 192 ms (28%, p < 0.01). In addition, quinidine and verapamil had a characteristic "rate-smoothing" effect on atrioventricular conduction during atrial fibrillation. The rhythm was converted to sinus rhythm after quinidine in 5 (25%) of 20 patients and after the combination of quinidine and verapamil in 11 (55%) of 20 patients. Amiodarone restored sinus rhythm in 12 (60%) of 20 patients. Overall, a shorter duration of atrial fibrillation (p < 0.05) and a smaller left atrial size (p < 0.01) were predictive of successful conversion of the arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

[The implantable cardioverter/defibrillator].

Despite all advances in the diagnosis and therapy of cardiovascular diseases, the mortality from malignant ventricular tachyarrhythmias is still a major health problem. In addition to established therapeutic strategies in the prevention of sudden cardiac death such as antiarrhythmic drug treatment, catheter ablation or antiarrhythmic drug treatment, cardioverter/defibrillator was introduced to clinical practice in 1980. The number of 50,000 overall implants reflects the current clinical status of the therapy with implantable cardioverter/defibrillators. Significant technical improvements in the defibrillator therapy may contribute to an increase in therapy acceptance. These advances include the introduction of nonthoracotomy lead systems, enhanced defibrillation efficacy, full programmable devices providing tiered electrical therapy, improved diagnostic Holter functions and enhanced arrhythmia detection algorithms. The major present goals of defibrillator therapy are detection and termination of malignant ventricular tachyarrhythmias, prevention of sudden cardiac death, reduction in patient's mortality and improvement in quality of life. The efficacy and safety of defibrillator therapy to prevent sudden arrhythmic death has been proven in several large clinical investigations In patients with this device the annual sudden cardiac death mortality is < 2% even in high-risk patient populations. Compared to sudden cardiac death rate there is a much higher rate of overall cardiac mortality because a defibrillator is not able to prevent nonarrhythmic cardiovascular deaths. There is a clinical impression that cardiovascular mortality is lower in patients treated with an implantable cardioverter/defibrillator compared to patients treated with other therapies. However, there are no results from controlled studies providing scientific evidence that defribillator therapy can decrease overall cardiovascular mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Death, Sudden, Cardiac↗
PubMed1994

[Myocardial vitality: clinical correlates and diagnostic concepts].

Modern therapeutic options in ischemic coronary disease such as thrombolysis, coronary angioplasty, new emerging strategies in treating heart failure and secondary prevention have resulted in decreasing cardiac mortality over the last ten years. In the era of interventional cardiology a new focus of clinical interest is the process of transition from loss of contractile function to definitive necrosis of severely ischemic myocardium. The decision for bypass surgery or angioplasty in patients with compromised contractile function should be based on evidence of viable myocardium with some or full potential for functional recovery; otherwise prognostic benefit may be questionable or dubious. The clinical substrate of non-contractile, but viable myocardial tissue may be present in patient presenting with both stable and unstable angina, in cases of acute or chronic myocardial infarction and in the setting of congestive heart failure resulting from ischemic cardiomyopathy. Various diagnostic methods are theoretically useful to assess residual myocardial viability both in hibernating myocardium (contractile down-regulation) and post-ischemic stunned (reperfused) myocardial tissue. Myocardial viability is confirmed both in presence of systolic wall motion or systolic wall thickening as evidenced from (contrast or radionuclide) left ventricular angiograms or echograms. Moreover, myocardial tissue perfusion by thallium-201 or other radioactive perfusion agents as documented by uptake of tracer is considered clear evidence of viability; however, lack of uptake of perfusion agents may not always exclude viable myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗