Anatomy for right ventricular lead implantation.

To understand the position of a pacing lead in the right ventricle and to correctly interpret fluoroscopy and intracardiac signals, good anatomical knowledge is required. The right ventricle can be separated into an inlet, an outlet, and an apical compartment. The inlet and outlet are separated by the septomarginal trabeculae, while the apex is situated below the moderator band. A lead position in the right ventricular apex is less desirable, last but not least due to the thin myocardial wall. Many leads supposed to be implanted in the apex are in fact fixed rather within the trabeculae in the inlet, which are sometimes difficult to pass. In the right ventricular outflow tract (RVOT), the free wall is easier to reach than the septal due to the fact that the RVOT wraps around the septum. A mid-septal position close to the moderator band is relatively simple to achieve and due to the vicinity of the right bundle branch may produce a narrower paced QRS complex. Special and detailed knowledge is necessary for His bundle and left bundle branch pacing.

Anatomy for atrial lead implantation.

Positioning and fixation of pacemaker leads in the right atrium depends on advanced anatomic knowledge in order to correctly interpret information from fluoroscopy and electrograms. Particularly the inability to reach a certain position or to achieve lead stability requires familiarity with right atrial structures such as the Eustachian ridge or areas of trabeculated versus smooth myocardium. Only a good understanding of right atrial anatomy makes it possible to replace electrophysiologically suboptimal atrial pacing sites such as right atrial appendage or high lateral wall by electrophysiologically better septal atrial pacing sites.

In-hospital complications in acute ST-elevation myocardial infarction depending on renal function.

BACKGROUND: To analyze in-hospital complications in patients with acute ST-elevation myocardial infarction (STEMI) depending on renal function. DESIGN: Observational study in patients with STEMI. METHODS: The study included 169 patients undergoing primary percutaneous coronary intervention. In all patients glomerular filtration rate (GRF) was calculated using the Modification of Diet in Renal Disease Study (MDRD) equation. Of these patients, 84 had a GFR ≥ 90 ml/min/1.73 m2 (Group 1) and 85 < 90 ml/min/1.73 m2 (Group 2). Other parameters in both groups were comparable. Study groups were followed to compare Killip class > 2 acute heart failure, in-hospital pneumonia, pulseless ventricular tachycardia or ventricular fibrillation, new onset atrial fibrillation, and high grade atrioventricular block. All patients were treated according to European Society of Cardiology (ESC) guidelines for the management of acute myocardial infarction in patients presenting with ST elevation. RESULTS: Mean GFR in Group 1 was 107.6 [Formula: see text] and in Group 2 75.3 [Formula: see text] 11.2 (p < 0.0001). The incidence of atrial fibrillation was higher in Group 2: in Group 1 and Group 2 the atrial fibrillation rate was 1.12% (one of 84) vs 8.24% (seven of 85) (p = 0.031), respectively. Group 1 revealed significantly lower rates of acute heart failure (Killip class > 2): in Group 1 and Group 2 0% (0 of 84 patients) vs 5.88% (five of 85 patients) (p = 0.024), respectively. The authors found no significant differences for other complications: in Group 1 and Group 2 ventricular tachycardia or ventricular fibrillation was 4.76% (four of 84 patients) vs 5.89% (five of 85 patients) (p = 0.75), high grade atrioventricular block was 2.38% (two of 84 patients) vs 4.71% (four of 85 patients) (p = 0.41), and the in-hospital pneumonia rate was 2.38% (two of 84 patients) vs 4.71% (four of 85 patients) (p = 0.41), respectively. CONCLUSION: Patients with lower GFR were more likely to suffer from in-hospital acute heart failure (Killip class > 2) and atrial fibrillation in STEMI despite primary percutaneous coronary intervention. Renal function did not affect in-hospital pneumonia, pulseless ventricular tachycardia or ventricular fibrillation rates. The evaluation of kidney function through GFR in STEMI patients may make in-hospital complications more predictable.

The role of anticoagulation in preventing myocardial infarction and improving outcomes in COVID-19 patients.

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with cardiovascular (CV) complications including myocardial injury, myocarditis, arrhythmias, and venous thromboembolism. The infection is more severe in patients with pre-existing cardiovascular disease (CVD), where systemic inflammation due to cytokine storm, hypercoagulation, as well as high hematocrit and platelet (PLT) count may contribute to an increased CV risk. The authors hypothesize that anticoagulants and antiplatelets prevent miocardial infarction (MI) in patients with pre-existing CVD. METHODS: A cohort study enrolled patients with a confirmed diagnosis of COVID-19. Clinical and laboratory data, total and CV mortality, as well as MI incidence and treatment regimens were compared according to the time of hospitalization: 40-day period in April-May (Group 1) and in October-November (Group 2). RESULTS: A total of 195 patients were enrolled: 93 in Group 1, with 36.5%, and 102 in Group 2 with 38.2% pre-existing CVD. Group 1 was managed with infusion therapy; only 10.7% received anticoagulation. Group 2 received preventive anticoagulants, antiplatelets, and infusion therapy. In Group 1, seven cases of MI were recorded compared to only three in Group 2. No significant difference in overall mortality (4.3% vs 6.86%, p = 0.441) and MI incidence (7.5% vs 2.9%, p = 0.149) was found, but significant differences were seen in the incidence of severe and critically ill cases between the groups (69.9% and 7.5% vs 75.5% and 20.6%, p < 0.001). CONCLUSIONS: Poorer outcomes in the early COVID-19 wave were associated with inadequate anticoagulation due to lack of knowledge about the new virus. Despite significantly more severe cases, there was no significant difference in overall mortality and MI incidence in patients with anticoagulation.

Atrial Fibrillation in Patients with Embolic Stroke of Undetermined Source during 3 Years of Prolonged Monitoring with an Implantable Loop Recorder.

BACKGROUND: Undocumented atrial fibrillation (AF) is suspected as a main stroke cause in patients with embolic stroke of undetermined source (ESUS), but its prevalence is largely unknown. This prospective study therefore aimed at delineating the prevalence of AF in patients with ESUS using continuous cardiac monitoring by implantable loop recorder (ILR) with daily remote interrogation over a period of 3 years and its clinical consequences, including recurrent stroke. METHODS: In consecutive patients with an ESUS diagnosis after complete work-up, an ILR was implanted and followed by daily remote monitoring until AF was detected or a follow-up of at least 3 years was completed. Additionally, the ILR was interrogated in-hospital in 6-month intervals. RESULTS: A total of 123 patients (74 male, mean age 65 ± 9 years) were enrolled and completed the 3 years study period. AF was detected in 51 patients (41.4%). In 43 of the 51 AF positive patients (84%) oral anticoagulation was established. Recurrent strokes occurred in 18 patients (14.6%) of this ESUS population, 9 of these patients being AF positive (17.6% of the AF-positive patients) and 9 being AF negative (12.5% of AF-negative patients). Patients with AF were slightly older than patients without AF (63.1 ± 8.8 vs. 67.5 ± 9.6 years, p = 0.12). Other parameters such as CHA2DS2-VASc score, infarct localization, micro- and macroangiopathy, carotid or aortic plaques, or stroke recurrence were not significantly different between groups. CONCLUSION: In ESUS patients, early implantation of an ILR with cardiac monitoring and remote transmission over a 3-year period detected AF in 41.4% and resulted in oral anticoagulation in 84% of these patients.

[Pifalls in the interpretation of pacemaker ECGs]. / Pitfalls in der Interpretation von Schrittmacher-EKGs.

The analysis of the pacemaker ECG is usually regarded as difficult and may generate rather mediocre interpretations. It is a common opinion that a pacemaker ECG can only be analyzed if the type of pacemaker (single-, dual-, triple-chamber, manufacturer, model) and its programming are known. The following pitfalls illustrate how to achieve a clinically meaningful ECG interpretation in daily practice, even if these details are not known. A systematic approach to ECG interpretation is particularly crucial in this context: Basic rhythm (P waves, intrinsic or paced rhythm), paced QRS complex (axis, width, bundle branch block morphology), signs of pacemaker malfunction (under­/oversensing, loss of capture), arrhythmia to which the pacemaker reacts, or activity of any pacemaker algorithm. Many small details should not be overlooked and many questions can be answered if a few principles are applied. Understanding of the pacemaker ECG can improve the life of a device patient at the touch of a button.

[Cardiac electrical device therapy in heart failure]. / Kardiale elektrische Device-Therapie bei Herzinsuffizienz.

Heart failure is one of the most common reasons for inpatient treatment and one of the most common causes of death in Germany. In addition to coronary heart disease (ischemic cardiomyopathy, ICM), there are also numerous other diseases as non-ischemic cardiomyopathy, NICM. Chronic heart failure is the final stage of diseases with cardiac involvement and limits the prognosis and quality of life of patients. The course can be favorably influenced by cardiac implantable electrical devices (CIEDs). There are different uses of CIEDs which are shown in this article.

His bundle pacing: troubleshooting during follow-up.

Follow-up of pacemaker systems for His bundle pacing (HBP) requires electrocardiogram (ECG) knowledge and creative thinking. This relates to ventricular threshold measurement in which it can be difficult to distinguish between selective HBP and loss of capture with pseudofusion since, by definition, intrinsic QRS complexes and those selectively paced via the His bundle look identical. Threshold testing in HBP is best performed in unipolar pacing mode, recording of a 12-lead ECG and pacing in VVI mode significantly above the intrinsic rate. Peculiarities of HBP relate to oversensing by the His bundle lead of atrial activity or the His bundle potential itself, leading to ventricular asystole or incorrect measurements during sensing testing. Ventricular undersensing and the use of His bundle plus additional right ventricular leads may lead to complex ECGs. However, other daily pacemaker problems (such as tachycardia above the upper rate limit or premature beats) and specific phenomena (such as paradoxical cardiac memory) may also be demanding in ECG troubleshooting of HBP.

[Indications for His bundle and left bundle branch pacing]. / Indikationen zur His-Bündel- und Linksschenkelstimulation.

His bundle pacing (HBP) allows ventricular excitation through the entire cardiac conduction system, resulting in a better synchronicity and efficacy of contraction compared to myocardial pacing. Due to better, dedicated implantation tools and exact practical implantation recommendations, HBP has developed into a form of stimulation that can be successfully applied with reasonable time and effort in >90% of patients. The rate of lead dislodgement and threshold increase is similar to conventional pacemaker systems. Despite a rather weak data base and a paucity of randomized trials, HBS represents an alternative to conventional right or biventricular pacing in the following conditions: (1) high-degree atrioventricular (AV) block with expected ventricular pacing >20% of the time, (2) AV block 1st degree with long PQ (alone or in combination with intermittent 2nd to 3rd degree AV block or sick sinus syndrome), (3) AV node ablation due to refractory atrial fibrillation, and (4) upgrade in pacing-induced cardiomyopathy. Moreover, HBP may be useful in context with cardiac resynchronization therapy (CRT). Left bundle branch block below the level of His represents a limitation of HBP. Therefore, more recently left bundle branch pacing (LBBP) has been introduced to correct left bundle branch block. LBBP seems to be possible in a wider anatomic area and may be easier to implant. However, LBBP requires active screw-in of the lead deep into the ventricular septum. Experience with this new technique is limited, particularly regarding long-term performance.

His bundle pacing: troubleshooting at implantation.

His bundle pacing produces electrocardiograms (ECGs) that give the impression that it is physiological like no other form of cardiac pacing requiring ventricular stimulation. Several special features of the implantation technique of a His bundle lead that distinguish it significantly from the implantation of other endocardial leads need to be considered. This overview provides a number of practical "hands-on" tips and tricks, from implantation set-up (12-lead ECG, no electrophysiology unit, no His bundle catheter), venous access, handling of delivery catheters and leads, interpretation of intracardiac electrograms, fluoroscopy and the surface ECG, finding the optimal pacing site, and implantation of the lead to fine-tuning and troubleshooting of difficult implantations and lead dislodgement. This review should help to facilitate the implantation of His bundle leads, shorten the learning curve and help to improve implantation results.

Perservative paroxysmal atrioventricular block : Cardiac syncope misdiagnosed as anxiety for more than 20 years.

A 42-year-old woman was referred for cardiac diagnostic work-up of loss of recurrent consciousness over the past 25 years. She received medication with an anxiolytic, an antidepressant, and a neuroleptic drug. After a normal resting ECG, there were 112 episodes of paroxysmal atrioventricular block III° in her 24 h Holter recording with asystole for up to 27 s. The patient was symptomatic only once with dizziness due to an asystole of 8.8 s while she was awake in the early morning. After DDDR pacemaker implantation, the patient was asymptomatic during the following 2 years. This case illustrates the complex and not fully understood problem of paroxysmal AV block, in this instance neither intrinsic, nor phase 4 or vagally induced. It further reminds us to carefully clarify the cause of loss of consciousness consistently which may render prolonged ECG monitoring necessary also in patients without heart disease.