Cardiac chemoreflex sensitivity in critically ill patients.

Chemoreflexes are important mechanisms for regulating ventilatory and cardiovascular function. The aim of this study was to determine the meaning of autonomic dysfunction for the pathophysiology and outcome in critical ill patients. For the determination of the chemoreflex sensitivity (ChRS), the ratio of the RR interval shift and the shift of oxygen partial pressure during a 5-min inhalation of oxygen with a nose mask was formed. Pathological chemoreflex sensitivity was predefined as a ChRS below 3.0 ms/mmHg. Out of the 27 critical ill patients included into the study, 17 had a sepsis and 10 a cardiogenic shock. In these patients, chemoreflex sensitivity was significantly reduced compared with a control group (sepsis: 2.1 +/- 1.68, cardiogenic shock: 0.4 +/- 0.27, controls: 5.0 +/- 2.8 ms/mmHg; P<0.05 vs. sepsis or cardiogenic shock). There was a significant negative correlation (r=-0.6; P<0.01) between the chemoreflex sensitivity and the severity of illness described by the SOFA-score. We conclude that cardiac reflex mechanisms are changed toward increased sympathetic activity reflected by reduced chemoreflex sensitivity in critical ill patients. Moreover, there is a close negative correlation between the ChRS and the SOFA-score.

Obstructive sleep apnea in heart failure patients: evidence for persistent conduction disturbances or sinus node dysfunction.

Bradycardia is a common finding in patients with obstructive sleep apnea and might be pronounced in heart failure patients. The aim of the present study was to determine the relationship between nocturnal hypoxemia, apnea-hypopnea index, and electrophysiological parameters of sinus node and atrioventricular conduction properties. Electrophysiological studies were performed in 12 patients with heart failure. Polygraphic studies were done in all of the patients. Patients with an AHI >10/h were classified as sleep apnea patients. Mild sleep apnea was diagnosed in 50% of the patients (AHI 17.8 +/- 4.4 vs. 5.1 +/- 3.6/h). There were no differences with respect to the resting heart rate, PQ interval, or QRS duration between the two groups. Sinus node recovery time was normal in all of the patients (993 +/-291 vs. 1099 +/-62 ms, P=0.45). There was no abnormal atrioventricular conduction. Nevertheless, sleep apnea patients showed decreased atrioventricular conduction time (AH) intervals (134 +/- 42 vs. 102 +/- 25 ms, P=0.1) and infranodal conduction time (HV) intervals (59 +/- 9 vs. 43 +/- 7 ms, P=0.01). We conclude that mild sleep apnea was not associated with abnormal findings in sinus node function or AV conduction properties in patients with heart failure. Decreased AH/HV intervals might be a consequence of apnea associated sympathetic activation.

[Hypertension and cardiac failure]. / Hochdruck und Herzinsuffizienz.

Arterial hypertension is the leading cause of mortality and morbidity with a worldwide prevalence of 26%. Aging increases the incidence of arterial hypertension. Arterial hypertension is the prime example for a chronic disease with asymptomatic beginning, creeping course and fatal outcome. Arterial hypertension is a major cardiovascular risk factor and leads to vascular as well as myocardial manifestations: coronary artery disease, hypertensive microvascular disease, concentric left ventricular hypertrophy as well as perivascular and interstitial fibrosis. In the late stages of the disease, hypertrophy and cardiac failure develop. Arterial hypertension is the leading cause of coronary artery disease and cardiac failure, and coronary artery disease is the cause of heart failure in 50% of cases. Various non-invasive and invasive procedures are available for screening and follow-up. The primary therapeutic target is to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms as well as lowering blood pressure. This article covers the pathophysiology of arterial hypertension and cardiac failure, clinical symptoms, diagnostic options and therapeutical goals as well as medicinal options.

[The heart in hypertension]. / Das Herz bei arterieller Hypertonie.

The term hypertensive heart disease covers the entities of left ventricular hypertrophy, microangiopathy and endothelial dysfunction resulting in diastolic and systolic dysfunction, arrhythmias and increased cardiovascular risk. From the pathophysiological point of view, this is caused by the hypertrophy of cardiac myocytes, interstitial fibrosis and media hypertrophy of the arterioles. Microangiopathy can be diagnosed as the earliest sign of hypertensive heart disease, with diastolic dysfunction also being found as an early change. In further persisting arterial hypertension left ventricular hypertrophy develops (often asymmetric) and later a systolic dysfunction. Clinically, the patients suffer from angina pectoris, dyspnea and rhythm disorders. Left ventricular hypertrophy is associated with an increased risk of malignant ventricular arrhythmias. Thus, the main therapeutic principle should be antihypertensive therapy with the goal of regression of hypertrophy leading to decreased mortality risk.

[Right atrial ablation of ectopic atrial tachycardia using a 20-pole mapping catheter]. / Ablation ektoper rechtsatrialer Tachykardien unter Verwendung eines 20-poligen Mapping-Katheters.

INTRODUCTION: Ectopic atrial tachycardia (EAT) are frequently unresponsive to pharmacological antiarrhythmic therapy. Radiofrequency ablation seems to be a safe approach to treat those arrhythmias. In the present study we report our results of radiofrequency ablation of EAT with a new mapping system (Stablemapr, Medtronic). METHODS: Thirty consecutive patients with right atrial tachycardia were included in the study. In 15 patients (G1) the 20-polar Stablemapr was used for localization of the arrhythmia foci. Data were compared with a control group (G2, n=15), in which mapping was performed conventionally. The demographic characteristics and the distribution of the different cardiac diseases were comparable in both groups. In group 1 the identification of the EAT was facilitated by the placement of the 20-pole mapping catheter in the right atrium. In group 2 point by point measurements were performed to find the earliest local atrial activation compared to a reference electrode in the high right atrium (activation mapping), or foci were identified by analysis of the P-wave morphology during stimulation (pacemapping). RESULTS: It was possible to successfully ablate all atrial tachycardias. The distribution of the foci was similar in both groups (G1/G2): near to the superior (3/5) and inferior (1/0) caval vene ostium, on the free wall (3/3), at the coronary sinus ostium (3/3) and on the interatrial septum (5/4). The mean procedure (G1: 88+/-33 vs G2: 151+/-61 min; p= or <0.05) and fluoroscopic times (G1: 19+/-9 vs G2: 38+/-28 min; p= or <0.05) were significantly shorter in group 1. Moreover, the mean number of radiofrequency applications was reduced significantly by using the new mapping system (G1: 10+/-10 vs G2: 16+/-13; p= or <0.05). CONCLUSION: Radiofrequency ablation of EAT with right atrial focus can be performed safely and successfully using a 20-pole mapping catheter. The greatest advantages compared to conventional mapping and ablation strategies lies in the shortened investigation and fluoroscopic time.

[Atrial fibrillation]. / Vorhofflimmern.

Atrial fibrillation represents the arrhythmia that most frequently leads to hospital admission. Due to the age structure of our population and the increasing morbidity and comorbidity, one has to assume that this arrhythmia will reach an even higher prevalence. The therapeutic successes are often insufficient. First of all, it is important to diagnose and treat the underlying disease. Secondly, antiarrhythmic therapy has to be considered in symptomatic patients. In those patients and in the case of a persistent form, electrical cardioversion should be performed. Repetitive cardioversions in asymptomatic patients yield no advantage for mortality. Antiarrhythmic therapy consists of drugs of the classes Ia, Ic, and III. Concomitant anticoagulation is necessary; ASS in indicated only in patients without structural heart disease and lacking thromboembolic risk factors. If risk factors are present, effective therapy with coumarin derivatives is required. Therapy with ACE inhibitors and AT blockers leads to an advantage in patients with arterial hypertension and/or heart failure concerning the stability of sinus rhythm after cardioversion and the incidence of arrhythmia. Newer medications for anticoagulation and newer antiarrhythmic drugs raise the hope of a future therapy with higher efficacy and lower rate of side effects.

[Cardiovascular end organ impairment due to hypertension]. / Kardiovaskuläre Endorganschäden des Hochdrucks.

Arterial hypertension is the most frequent cause of pressure overload on the left ventricle. Longer lasting arterial hypertension leads to hypertension-specific organ manifestations summarized as "hypertensive heart disease". Hypertensive heart disease comprise the manifestation of stenosis in epicardial arteries, hypertensive microvascular disease, ischemic cardiomyopathy, left ventricular hypertrophy, endothelial dysfunction, increased sympathetic drive and degeneration of aortic valve. Diastolic dysfunction and reduced coronary flow reserve can be evaluated as early markers of hypertensive heart disease. These alterations lead to the major clinical manifestations of hypertensive heart disease that are symptoms of reduced coronary insufficiency with typical angina pectoris, but also of symptoms of heart failure (systolic and diastolic dysfunction) and arrhythmia. Different non-invasive and invasive procedures are available for screening and follow-up of patients with hypertensive heart disease. Primary therapeutic target is, apart from lowering blood pressure, to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms.

Disseminated microvascular pulmonary tumor cell embolism: a rare cause of fulminant pulmonary hypertension.

BACKGROUND: Disseminated pulmonary tumor embolization is a rare cause of pulmonary hypertension and is often diagnosed only after the patient has died. CASE REPORT: We report on a 41-year-old male who was admitted because of severe dyspnea and tachycardia. Contrast enhanced spiral computed tomography did neither establish pulmonary thromboembolism nor pulmonary metastasis. Right heart catheterization revealed severe pulmonary hypertension (pulmonary vascular resistance (PVR) 678 dyn x sec x cm(-5)). PVR did not respond to therapy with intravenous nitrate or inhaled iloprost in this critically ill patient. 2 days after admission, the patient died because of refractory right heart failure. Autopsy revealed microscopic pulmonary tumor embolism due to a metastasizing adenocarcinoma of the pancreas. CONCLUSION: Disseminated tumor cell embolism should be considered as a rare differential diagnosis in patients with refractory pulmonary hypertension.

[Determinants of paroxysmal atrial fibrillation in patients with arterial hypertension]. / Determinanten des paroxysmalen Vorhofflimmerns bei Patienten mit arterieller Hypertonie.

INTRODUCTION: Atrial fibrillation represents an important arrhythmia, in particular in patients with arterial hypertension. Hitherto, the connection between paroxysmal atrial fibrillation, left atrial size and left ventricular muscle mass has not been investigated sufficiently. In the present study, determinants of paroxysmal atrial fibrillation in patients with arterial hypertension were evaluated. METHODS: 104 consecutive patients were enrolled into this study. All of them suffered from arterial hypertension for more than one year. Persistent or permanent atrial fibrillation was not documented. In all of these patients, clinical, echocardiographic and rhythmologic variables were evaluated. RESULTS: In 10.3% of the patients, paroxysmal atrial fibrillation was found. These patients showed a significantly larger left atrium (43.3 +/- 6.7 vs 37.5 +/- 4.9 mm, p < 0.001), a significantly higher muscle mass of the left ventricle (152.38 +/- 43.57 vs 134.41 +/- 27.19 g/m2, p < 0.01) and significantly more frequent a mild mitral regurgitation (38.1 vs 28.6%, p < 0.01). The multivariate regression analysis revealed as independent factors for paroxysmal atrial fibrillation the size of the left atrium and the presence of mild mitral regurgitation. Independent factors for an enlarged left atrium were mitral insufficiency and left ventricular muscle mass. CONCLUSION: This study shows that paroxysmal atrial fibrillation in aterial hypertension is based on the left atrial size, and left atrial size on left ventricular muscle mass. Therefore, these results should lead to a causal therapy for treatment of paroxysmal atrial fibrillation in these patients.

[Long-term follow-up of right atrial multilinear high-frequency ablation in the treatment of recurrent paroxysmal atrial fibrillation]. / Langzeitverlauf nach rechtsatrialer, multilinearer Hochfrequenzablation zur Behandlung von rezidivierendem paroxysmalem Vorhofflimmern.

BACKGROUND AND OBJECTIVE: To investigate the long-term follow-up after right atrial compartmentalization using radiofrequency catheter ablation to treat recurrent paroxysmal atrial fibrillation. PATIENTS AND METHODS: 33 patients (eight women / 25 men, mean age 56.1+/-9.9 years) with highly symptomatic recurrent paroxysmal atrial fibrillation and mostly unresponsive to antiarrhythmic drugs were enrolled in this prospective study. All patients underwent radiofrequency catheter ablation, including right atrial compartmentalization and ablation of the right atrial isthmus region. The primary goal during follow-up was documentation of arrhythmia-related symptoms using a SF-36 quality-of-life questionnaire. RESULTS: During a mean follow-up of 2.1 years 21 % of patients were free of a relapse under continued antiarrhythmic medication, 79 % suffered at least from one period of atrial fibrillation. According to the underlying heart disease patients classified as "lone atrial fibrillation" (40 % without a relapse) showed improvement particularly compared to patients with coronary heart disease (10 % without a relapse). In the group of patients with a relapse of atrial fibrillation the mean of duration of an arrhythmic episode decreased significantly from 10.6 to 2.3 hours under continued administration of antiarrhythmic drugs (p = 0.01), as did the number of episodes, from 2.2 to 1.9/week. CONCLUSION: Despite of the high rate of clinical relapse, patients can profit due to an improved responsiveness to antiarrhythmic drugs after ablation. Right atrial compartmentalization should not be understood as a causal therapy but as an approach to a symptomatic form of hybrid therapy.

Chemoreflexsensitivity in chronic heart failure patients.

AIMS: Patients with heart failure are characterised by a disturbed sympathovagal balance, as could be shown by analyses of heart rate variability and baroreflexsensitivity. Furthermore, the modulation of ventilation is disturbed in those patients with an increased ventilation volume following the inhalation of hypoxic gas. This study should evaluate, whether heart failure patients have a decreased hyperoxic chemoreflexsensitivity associated with an increased rate of ventricular arrhythmias. METHODS AND RESULTS: Into this study, 49 consecutive patients were enrolled. Of these, 23 suffered from heart failure; the remaining had no evidence of heart failure and a normal left ventricular ejection fraction. All patients were investigated by analysing the reduction of heart rate following inhalation of pure oxygen. The difference of RR-interval divided by the difference of the venous oxygen partial pressure both before and after oxygen inhalation resulted in the chemoreflexsensitivity. Patients with heart failure showed a significantly decreased chemoreflexsensitivity compared to those without (2.62+/-1.85 vs. 5.80+/-6.37 ms/mmHg, P<0.05). Of patients with heart failure, 69.6% had a decreased chemoreflexsensitivity below 3 ms/mmHg, in contrast to only 38.5% of the control group. Patients with decreased chemoreflexsensitivity showed significantly more non-sustained ventricular tachycardias (46 vs. 4%, P<0.05) during Holter ECG. CONCLUSION: Patients with heart failure show a significantly decreased hyperoxic chemoreflexsensitivity. A decreased chemoreflexsensitivity is associated with an increased rate of non-sustained ventricular tachycardias. This may be related to an increased sympathetic tone in these patients. The chemoreflexsensitivity may be important in arrhythmic risk stratification of patients with heart failure.

T wave alternans and ventricular arrhythmias in arterial hypertension.

Patients with a positive microvolt-level T wave alternans (TWA) are characterized by an increased risk of ventricular tachyarrhythmias. Arterial hypertension leads to an increase of sudden cardiac death risk, particularly if left ventricular hypertrophy is present. The aim of this study was to investigate the value of TWA in patients with arterial hypertension. Fifty-one consecutive patients were included in the study. TWA analysis was performed with patients sitting on a bicycle ergometer and exercising with a gradual increase of workload to maintain a heart rate of at least 105/min. After recording 254 consecutive low-noise-level heartbeats, the exercise test was stopped. The ECG signals were digitally processed by a spectral analysis method. The magnitude of TWA was measured at a frequency of 0.5 cycle per beat. A TWA was defined as positive if the ratio between TWA and noise level was >3.0 and the amplitude of the TWA was >1.8 microV. Eight of the 51 patients (16%) showed a positive TWA. If left ventricular hypertrophy was present, the prevalence of TWA was higher (33.3% versus 8.3%; P:<0.05). Sensitivity concerning a previous arrhythmic event was 73%, and specificity was 100%. The alternans ratio was significantly higher in patients with a previous event (39.3+/-62.3 versus 2.4+/-4.6; P:<0.001), as was the cumulative alternans voltage (4.7+/-4.1 versus 1.6+/-1.9 microV; P:<0.001). In 16 patients invasively investigated by an electrophysiological study, a significant correlation between inducibility of tachyarrhythmias and a positive TWA result was found (Spearman R:=0.36, P:=0.01). We conclude that the arrhythmic risk of patients with arterial hypertension is markedly increased if microvolt-level TWA is present. The prevalence of TWA is higher in patients with left ventricular hypertrophy.

Arterial hypertension and cardiac arrhythmias.

PURPOSE AND DATA IDENTIFICATION: One of the main clinical problems of patients with arterial hypertension is the presence of arrhythmias, especially if left ventricular hypertrophy exists. Recent results from our group and all data available via Med-Line-search have been analysed. The analysis was focused on atrial and ventricular arrhythmias and arrhythmic risk prediction, using non-invasive markers. RESULTS OF ANALYSIS AND CONCLUSION: Arterial hypertension is a major cause of non-rheumatic atrial fibrillation and other supraventricular arrhythmias. The prevalence of ventricular arrhythmias is increased in hypertensive patients without left ventricular hypertrophy, compared to normotensives. If left ventricular hypertrophy is present, the risk for ventricular tachycardias is quadrupled. The presence of left ventricular hypertrophy is associated with an increase in all-cause mortality by a factor of seven in men and nine in women. In particular, patients with hypertrophy, increased rate of ventricular extrasystoles up to non-sustained ventricular tachycardia and ST-depression in long-term ECG are threatened by sudden cardiac death. At present, it is not possible to safely identify patients with increased risk. Regression of hypertrophy exists along with a decreased rate of ventricular extrasystoles. We hypothesize that by the regression of hypertrophy, the prevalence of sustained ventricular tachycardia decreases and therefore the prognosis of those patients can be improved, although controlled studies are not yet available.

T wave alternans as a risk predictor in patients with cardiomyopathy and mild-to-moderate heart failure.

The analysis of t wave alternans (TWA) was introduced to identify patients with an increased risk of ventricular tachyarrhythmias. The inducibility of ventricular tachyarrhythmias and the spontaneous arrhythmic events are correlated with a positive TWA in patients with a reduced left ventricular ejection fraction and survived myocardial infarction. In contrast, this study is the first to investigate the correlation of a survived sudden cardiac death and TWA in patients without coronary heart disease and only slightly decreased left ventricular function. Sixty patients were included in the study. The TWA analysis was performed using the Cambridge Heart system (CH2000). Patients were sitting on a bicycle ergometer and exercised with a gradual increase of workload to maintain a heart rate of at least 105 beats/min. The exercise test was stopped after recording 254 consecutive low noise level heart beats. The electrocardiographic signals were digitally processed using a spectral analysis method. The magnitude of TWA was measured at a frequency of 0.5 cycles/beat. A TWA was defined as positive if the ratio between TWA and noise level was > 3.0 and the amplitude of the TWA was > 1.8 microV. Twelve (20%) of the included 60 patients showed a positive TWA. The sensitivity concerning a previous arrhythmic event amounted to 65%, the specificity up to 98%, respectively. The alternans ratio was significantly higher in patients with a previous event (30.3 +/- 53.2 vs 2.9 +/- 5.9, P < 0.001) and cumulative alternans voltage (4.67 +/- 3.55 vs 1.75 +/- 1.88 microV, P < 0.001). In 19 patients, invasively investigated by an electrophysiological study, a significant correlation between inducibility of tachyarrhythmias and a positive TWA result was found (Spearman R = 0.51, P = 0.01). In conclusion, the TWA analysis seems to identify patients with nonischemic cardiomyopathy who are at an increased risk of ventricular tachyarrhythmias.

[Cardiac complications in diabetes mellitus]. / Kardiale Beteiligung bei Diabetes mellitus.

Diabetes mellitus as a disease of epidemiological impact leads to diabetic cardiopathy by modulation of myocardial, vascular and metabolic components. This includes the development of a coronary microangiopathy and a decrease of diastolic and systolic function of the left ventricle as well as the development of an autonomic diabetic neuropathy. Patients with diabetes show an increased mortality concerning cardiovascular events. They more often suffer from myocardial infarction as non-diabetics mostly with a more serious course. Moreover, the post-infarction course is affected with a worse prognosis as in non-diabetics. For diagnosis of cardial involvement in diabetes electrocardiographic and echocardiographic procedures are of use. Special tests of the autonomic function complete the diagnostic ensemble. An early therapy with ACE-inhibitors and beta blocking agents as well as a strong diabetes therapy, in particular with insulin, can influence the mortality favorably. Moreover, the diagnosis and therapy of additional cardiovascular risk factors (arterial hypertension, dyslipidemia) are very important, because these are correlated with a for diabetic patients markedly increased risk of mortality. The clinical relevance of the term diabetic cardiopathy is justified by the 6 factors: macroangiopathy, microangiopathy, disturbances of the myocardial metabolism, myocardial fibrosis, autonomic diabetic neuropathy and disturbances of the coagulability. Diagnostic and therapeutic goals are discussed.

Chemoreflexsensitivity in patients with survived sudden cardiac arrest and prior myocardial infarction.

For evaluation of patients with an increased risk of sudden cardiac death, the analyses of ventricular late potentials, heart rate variability, and baroreflexsensitivity are helpful. But so far, the prediction of a malignant arrhythmic event is not possible with sufficient accuracy. For a better risk stratification other methods are necessary. In this study the importance of the ChRS for the identification of patients at risk for ventricular tachyarrhythmic events should be investigated. Of 41 patients included in the study, 26 were survivors of sudden cardiac arrest. Fifteen patients were not resuscitated, of whom 6 patients had documented monomorphic ventricular tachycardia and 9 had no ventricular tachyarrhythmias in their prior history. All patients had a history of an old myocardial infarction (> 1 year ago). For determination of the ChRS the ratio between the difference of the RR intervals in the ECG and the venous pO2 before and after a 5-minute oxygen inhalation via a nose mask was measured (ms/mmHg). The 26 patients with survived sudden cardiac death showed a significantly decreased ChRS compared to those patients without a tachyarrhythmic event (1.74 +/- 1.02 vs 6.97 +/- 7.14 ms/mmHg, P < 0.0001). The sensitivity concerning a survived sudden cardiac death amounted to 88% for a ChRS below 3.0 ms/mmHg. During a 12-month follow-up period, the ChRS was significantly different between patients with and without an arrhythmic event (1.64 +/- 1.06 vs 4.82 +/- 5.83 ms/mmHg, P < 0.01). As a further method for evaluation of patients with increased risk of sudden cardiac death after myocardial infarction the analysis of ChRS seems to be suitable and predicts arrhythmias possibly more sensitive than other tests of neurovegetative imbalance. The predictive importance has to be examined by prospective investigations in larger patient populations.