Unusual echocardiographic evidence of hypercoagulation in usual left atrial appendage as the first and only sign of COVID-19.

Coronavirus disease 2019 (COVID-19) is a condition caused by a novel virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease's course ranges from entirely asymptomatic to severely ill patients. Hypercoagulation is often a complication of this disease, worsening the prognosis, which is extremely important in patients at higher risk of thromboembolic events, such as atrial fibrillation (AF), where thrombus formation in the left atrial appendage (LAA) is frequent. LAA could be of various sizes, volumes, and shapes, distinguish several morphologies, from which the WindSock LAA is the most frequent. In contrast, thromboembolic complications occur most frequently in patients with AF and the Cactus LAA. We present a clinical case of a 70-year-old woman with an initial negative real-time polymerase chain reaction (RT-PCR) test for SARS-CoV-2, suspicion of device-related infection after dual pacemaker implantation, AF, and LAA without thrombus in the initial transoesophageal echocardiography (TEE). Despite apixaban treatment, spontaneous restoration of sinus rhythm, and WindSock LAA morphology, the sludge in LAA was diagnosed in control TEE. The patient did not present any typical clinical COVID-19 symptoms but re-checked the RT-PCR test for SARS-CoV-2 infection was positive. The described case presents echocardiographic evidence of hypercoagulation as the first and only feature of SARS-CoV-2 condition besides the usual morphological presentation of the WindSock LAA.

Influence of hereditary haemochromatosis on left ventricular wall thickness: does iron overload exacerbate cardiac hypertrophy?

BACKGROUND: The left ventricular (LV) hypertrophy increases the risk of heart failure. Hypertension and infiltrative cardiomyopathies are the well-known reasons of LV hypertrophy. The growing interest of scientists in this issue affects hereditary haemochromatosis (HH), which is characterised by the excess deposition of iron mostly due to HFE gene mutation. The aim of our study was to investigate the possible influence of HH on LV parameters in patients with early-diagnosed (early HH) and long-lasting and long-treated (old HH) disease. MATERIALS AND METHODS: Thirty nine early HH and 19 old HH patients were prospectively enrolled in the study; age- and sex-matched healthy volunteers constituted the appropriate control groups. All participants had echocardiography performed (including three-dimension volume and mass analysis); the iron turnover parameters were measured at the time of enrolment in every HH patients. RESULTS: Echocardiographic parameters regarding to left atrium (LA), LV thickness, mass and long axis length were significantly higher, whereas LV ejection fraction was lower in early HH in comparison to healthy persons. In old HH patients the differences were similar to those mentioned before, except LV ejection fraction. The presence of hypertension in both HH groups did not influence echo parameters, as well as diabetes in old HH. The strongest correlation in all HH group was found between the time from HH diagnosis and LA, LV thickness and volumes parameters, but the correlations between iron turnover and echo parameters were non-existent. CONCLUSIONS: Hereditary haemochromatosis, not only long-lasting, but also early-diagnosed, could lead to exacerbation of LV wall thickness and cardiac hypertrophy. This effect is not simply connected with hypertension and diabetes that are frequent additional diseases in these patients, but with the time from HH diagnosis.

Modulation of AMP deaminase in rat hearts subjected to ischemia and reperfusion by purine riboside.

Changes in AMP deaminase (AMPD) activity influence heart function and progression of heart disease, but the underlying mechanism is unknown. We evaluated the effect of purine riboside (Purr) on the activity of AMPD in perfused rat hearts and in isolated rat cardiomyocytes. Brief perfusion of the pre-ischemic heart with 200 micro M Purr resulted in activation of AMPD, more pronounced degradation of the adenine nucleotides, and reduced recovery of the adenine nucleotide pool during reperfusion. Brief incubation of rat cardiomyocytes with 200 micro M Purr also activated AMPD, while prolonged exposure resulted in enzyme inhibition. We conclude that Purr activates AMPD, whereas metabolites of this compound may inhibit the enzyme.

Assessment of baroreflex sensitivity in patients with preserved and impaired left ventricular function by means of the Valsalva manoeuvre and the phenylephrine test.

The purpose of the present study was to assess the agreement between measurements of baroreflex sensitivity (BRS) obtained by the Valsalva manoeuvre and by the phenylephrine test in patients with previous myocardial infarction and different degrees of left ventricular dysfunction. Patients with a previous myocardial infarction were enrolled consecutively into two groups according to their left ventricular ejection fraction (LVEF): 40% (n=52). All patients underwent BRS assessment by the phenylephrine technique (Phe-BRS) and by the Valsalva manoeuvre, with the latter using both the overshoot part of phase IV (Ov-VM-BRS) and the whole of phase IV (IV-VM-BRS). The linear association between methods was assessed by correlation analysis and the agreement was evaluated by computing the bias and the limits of agreement. IV-VM-BRS and Ov-VM-BRS could not be computed in 26% and 39% of patients respectively. For both indices a much higher percentage of non-computable Valsalva manoeuvre slopes was found in the group of patients with LVEF 40% the results were: r=0.91 (P<0.001), bias=0.1 ms/mmHg (P=0.84) and limits of agreement from -4.8 to 5 ms/mmHg. When comparing Phe-BRS and IV-VM-BRS, we found r=0.67 (P=0.001), bias=-1.5 ms/mmHg (P=0.06) and limits of agreement from -8.8 to 5.7 ms/mmHg in the group of patients with LVEF 40%. Dichotomizing Ov-VM-BRS, the best cut-off value to identify patients with a Phe-BRS of <3 ms/mmHg was found to be 7 ms/mmHg, giving 100% sensitivity and 69% specificity. In conclusion, estimation of BRS by the Valsalva manoeuvre in post-myocardial infarction patients is limited by a large number of non-measurable results. When computable, measurements are well correlated with those obtained by Phe-BRS, but, because of large limits of agreement, the two methods cannot be used interchangeably. If used as a screening test for risk stratification, the Valsalva manoeuvre could reduce by about one-third the need for phenylephrine injection.

Arterial baroreflex modulation of heart rate in patients early after heart transplantation: lack of parasympathetic reinnervation.

BACKGROUND: Orthotopic heart transplantation results in cardiac denervation. The presence of cardiac parasympathetic reinnervation in humans has been widely debated based on the application of differing indirect measures of autonomic control. However no attempt has been made to analyse the reflex heart rate response to baroreceptor stimulation whose occurrence is generally considered a reliable marker of the ability to activate cardiac vagal reflexes. This study tested the hypothesis that the presence of donor heart RR interval lengthening following phenylephrine induced blood pressure increase would be an index of parasympathetic reinnervation. METHODS: Baroreflex sensitivity (BRS) was assessed in 30 patients (mean age 51+/-12 years) 1-24 months after heart transplantation carried out by the standard Lower-Shumway technique. In 6 patients the recipient atrium rate response (P-P interval) to baroreceptor stimulation by phenylephrine was also simultaneously determined by transesophageal recording. RESULTS: None of the 30 patients showed prolongation of RR intervals in the donor heart. The average BRS value was -0.28+/-0.54 ms/mmHg (range -1.3-0.7 ms/mm Hg). In the 6 patients in whom BRS was obtained at both the recipient atrium (P-P) and donor heart (R-R) the changes were 7.6+/-5.7 ms/mm Hg and -0.38+/-0.58 ms/mm Hg respectively (p = 0.02), thus confirming that the absent RR interval lengthening in the donor heart is the consequence of efferent vagal fiber interruption. CONCLUSIONS: The absence of any RR interval prolongation following phenylephrine induced baroreceptor stimulation demonstrates that vagal efferent reinnervation of the donor heart does not occur up to 24 months in patients operated via the standard Lower-Shumway procedure. It is also suggested that analysis of baroreceptor reflexes is a more specific method in the examination of cardiac parasympathetic reinnervation.

Electrical atrial remodeling assessed by monophasic action potential and atrial refractoriness in patients with structural heart disease.

UNLABELLED: The present study was performed to assess the effect of induced atrial fibrillation (AF) on atrial monophasic action potentials (MAPs) and atrial refractory period (ERP) in patients with structural heart disease. An electrode MAP catheter was placed in the right atrium to continuously measure atrial potential duration (APD90) in 13 patients (coronary artery disease, 10 patients; dilated cardiomyopathy, 2 patients; hypertrophic cardiomyopathy, 1 patient) without spontaneous AF episodes. AF was induced by rapid atrial stimulation (300-1500/min). If sinus rhythm returned within 10 minutes, AF was reinduced. The atrial ERP was measured during atrial pacing at a basic cycle length of 550 ms before AF induction and after its conversion. RESULTS: The mean atrial ERP and the atrial APD90 before AF was 242 +/- 34 ms and 256 +/- 23 ms, respectively. ERP and APD90 shortening was observed after 3 minutes of AF. After 11 +/- 0.5 min (10 min 20 s-13 min 10 s) of AF, ERP and APD90 reached their minimal values of 72% +/- 13% and 71% +/- 10% of baseline, respectively. ERP and APD90 returned to their initial values within 10 minutes after conversion of AF. A tendency toward longer duration of consecutive AF episodes and facilitation of their induction was observed. CONCLUSION: The present study confirms that short episodes of AF modify the electrophysiological properties of the atria in humans. In patients with structural heart disease, induced atrial fibrillation shortens the atrial ERP as well as the atrial APD90. The changes were reversible within 10 minutes after arrhythmia termination.

[Left ventricular stroke volume in individuals with dual chamber pacemaker (DDD). Effect of atrioventricular delay]. / Objetosc wyrzutowa lewej komory serca u osob z wszczepionym stymulatorem typu DDD. Wplyw czasu opóznienia przesionkowo-komorowego.

UNLABELLED: Programming of atrioventricular delay in patients with dual chamber pacemaker is very important for left ventricular filling and has a consequence for its stroke volume. The aim of this study was to evaluate the influence of atrioventricular delay for left ventricular stroke volume during pacing at two different rates. The study was performed in 36 patients with DDD pacemaker aged from 30 to 81 years, mean 56.1 +/- 14.6. Using Doppler echocardiography we have assessed left ventricular stroke volume during two pacing rates (70 and 100 ppm) with four atrioventricular delays (100, 150, 200 and 250 ms). We have found statistically significant difference between stroke volume with various atrioventricular delays. During pacing rate of 70 ppm the maximal difference was 19% and 15% during 100 ppm. Comparing both pacing rates the distributions of hemodynamically optimal atrioventricular delays was also significantly different. The best atrioventricular delay from the hemodynamic point of view was 36 ms longer during 70 ppm of pacing rate than during 100 ppm (p = 0.0009). The most often optimal delay at 70 ppm was 190-200 ms, and the rarest optimal delay was 90-100 ms; during 100 ppm pacing respectively: 140-150 ms and 240-250 ms. We have observed considerable personal variability in the hemodynamic response for atrioventricular delay changing as well as in the hemodynamically optimal values of this parameter during both pacing rates. CONCLUSIONS: 1. Atrioventricular delay programming has significant influence on left ventricular stroke volume. 2. Programming of atrioventricular delay should be performed individually in every patient because of personal variability of optimal values of this parameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrioventricular conduction disturbances in patients with sinoatrial node disease and atrial pacing.

In sinoatrial node disease (SND) atrial pacing may be limited by progression of AV block. The incidence of AV block after AAI systems implantation range, according to various authors, from 0% to 12%. The aim of this study was to examine the AV conduction disturbances that forced a change in the mode of pacing in patients with AAI pacemakers. The information was collected retrospectively from a cohort of 122 patients. The follow-up period ranged from 5 to 83 months (mean = 35). Among these patients there were 37 with sinus bradycardia and 85 with bradycardia-tachycardia syndrome. Their mean age was 63 years. Before AAI pacemaker insertion, all patients had normal AV conduction on 12-lead ECG, and all but five had a Wenckebach cycle length shorter than 500 msec. Seven out of these 122 patients (5.7%) developed symptomatic conduction disturbances (second-degree type I AV block in five, second degree type II AV block in one, and third-degree AV block in one), necessitating a change from AAI to another mode of pacing. We conclude that progression of AV block after atrial pacemaker implantation in patients with SND is infrequent and mild in the majority of cases. Intraventricular disturbances such as left anterior hemiblock represent contraindication to AAI pacing particularly in patients who may be in need of antiarrhythmic drugs.

[Transesophageal stimulation of the left cardiac atrium in treatment of atrial flutter]. / Stymulacja przezprzelykowa lewego przedsionka serca w leczeniu trzepotania przedsionków.

Transesophageal stimulation of the left cardiac atrium in the treatment of paroxysmal atrial flutter was assessed. An attempt of such a therapy in paroxysmal atrial flutter involved 20 patients. Cardiac atrium was stimulated with overdrive technique, with single or pair of stimuli and multiple impulses of various frequency and duration. Reversal to sinus rhythm was achieved in 10 patients (in 3 out of them through phase of atrial fibrillation transitory). Results confirm therapeutical value of the transesophageal stimulation of the left cardiac atrium in atrial flutter.

Left atrial size and wall motion in patients with permanent ventricular and atrial pacing.

It is well known that during permanent ventricular pacing atrial arrhythmias and embolic complications occur much more frequently in comparison to permanent atrial or sequential pacing. Hemodynamic disturbances caused by ventriculoatrial conduction (VAC) are thought to be responsible for those complications. The aim of this study was to compare the left atrial size and its wall motion in three groups of patients with sick sinus syndrome. Group 1: 58 patients with VVI pacing and VAC observed (22 males, 36 females, aged 31-86, mean 62.3). Group 2: 43 patients with primary AAI pacing (13 males, 30 females, aged 27-74, mean 57.8). Group 3: 13 patients with AAI or DDD replacing the primary VVI mode due to pacemaker syndrome and/or heart failure, all with VAC present during VVI pacing (7 males, 6 females, aged 26-80, mean 59.8). Two-dimensional/M-mode echocardiography was performed in all these patients. In group 1 mean diastolic as well as mean systolic atrial diameters were significantly greater (P less than 0.005) and wall motion significantly smaller (P less than 0.005) in comparison to the other groups. Left atrial wall motion amounted to only 7.4% of the mean diastolic diameter in this group. Mean left atrial diastolic and systolic diameters and wall motion in patients with pacemakers preserving atrioventricular synchrony (group 2 and group 3) were almost identical and wall motion amounted to about 22% of the diastolic diameter in both these groups. We conclude that ventriculoatrial conduction leads to significant enlargement of left atrium and to the atrial wall-motion decrease. This predisposes to arrhythmias and embolic complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Transesophageal atrial pacing complications in patients suspected of tachy-brady syndrome.

The clinical effects of transesophageal atrial pacing (TAP) were assessed in 308 patients. Indications for TAP included evaluation for pacemaker implantation in patients suspected of sinus node dysfunction and determination of the suitable type of pacemaker. Most patients underwent program stimulation including rapid as well as burst stimulation. In one patient, following the study, cerebral arterial embolism occurred, most likely secondary to an induced arrhythmia. That was the only single case of permanent consequences following TAP. Additionally, one patient was accidentally stimulated in the ventricle using low voltage electric current that induced ventricular fibrillation. This was promptly reversed with defibrillation. Twenty-six patients in whom an arrhythmia was previously induced, required medical therapy, two of whom required cardioversion, and 24 required drug therapy, subsequent to clinical intolerance of the arrhythmia. No lethal complications occurred.

Transesophageal programmed atrial pacing as a method of selecting patients with sick sinus syndrome for permanent atrial pacing.

Many recent studies have shown transesophageal programmed atrial pacing (TP) as a very practical, safe and convenient way for assessment of sinus node function and AV conduction. On the other hand, permanent atrial pacing is known to be superior to ventricular pacing due to arrhythmogenic and hemodynamic reasons. This is the reason why we decided to use TP as a method of choosing patients with sick sinus syndrome (SSS) for permanent atrial pacing. Sixty-three patients with symptomatic (58) and asymptomatic (5) SSS in a variety of clinical situations were examined in this way. The following electrophysiological features were examined: sinus cycle length, sinus node recovery time as well as corrected time, secondary pause after overdrive stimulation, sinoatrial conduction time, Wenckebach point, induction of supraventricular arrhythmias by S1, S2, S3 programmed stimulation and burst pacing. Patients with abnormal parameters were examined once more after intravenous atropine 0.2 mg/kg to evaluate parasympathetic component. Standard 12-lead ECG was performed in all, and Holter monitoring in most of patients. Twenty-six patients were candidates for permanent AAI pacing. Failures occurred in eight patients usually due to low P wave amplitude and electrode instability. Eighteen patients received AAI pacing systems: eight with brady-tachycardia syndrome, nine with bradyarrhythmia and one with sinoatrial block. In the follow-up of 5-28 months in one patient occurred high degree AV block (II degree) during digitalis therapy. Reduction of doses made this block disappear. Examination of Wenckebach point and possibility of inducation of supraventricular tachyarrhythmias in cases of atrial overexcitability are particularly useful in selecting patients for AAI pacing.