Asystole Triggered by Swallowing: Insights From a Case of Infective Endocarditis in a 35-Year-Old HIV Patient

Introduction

Asystole is defined as the cessation of electrical and mechanical activity of the heart. The most common causes are deterioration of defibrillation rhythms such as ventricular fibrillation or pulseless ventricular tachycardia [1]. Asystole can cause sudden cardiac arrest (SCA) from primary causes due to heart disease (eg, myocardial infarction, heart failure, aortic stenosis) and secondary causes (eg, hypoxia, hypo/hyperkaliemia, hypovolemia, sepsis) [2]. The occurrence of asystole for several seconds, which may be associated with swallowing, is uncommon. To date, fewer than 150 such cases have been documented in the medical literature [3]. With regard to the nerve impulse during swallowing, impulses originating from the esophageal plexus are conveyed via the vagus nerve to the solitary band nucleus situated within the medulla oblongata. The signal that regulates esophageal peristalsis travels down the parasympathetic draining fibers via the esophageal branch of the vagus nerve. The presence of reflex arcs between the afferent sensory fibers and the efferent parasympathetic fibers of the cardiac branch results in inappropriate and excessive vagus nerve activation, which in turn causes bradycardia, disturbances to the conduction system, and hypotonia due to vasodilation. Excessive activation of the vagus nerve can result in cardiac inhibition. Asystole accompanying swallowing can be associated with diseases of the gastrointestinal tract (eg, hiatal hernia, esophageal stricture, achalasia and esophageal cancer), the cardiovascular system (eg, coronary artery disease, atrial fibrillation, sick sinus syndrome, aortic aneurysm, and rheumatic heart disease), or metabolic diseases (eg, hypertension, diabetes mellitus, dyslipidemia, and obesity) [4]. Additionally, neurological diseases can cause swallowing asystole, such as glossopharyngeal neuralgia, carotid artery stenosis, and metastatic brain tumors [5]. Infective endocarditis (IE) is an infection of the endothelium of the heart, which is caused by biological agents, most often bacteria. The inflammatory changes usually affect the valves, although other structures may also be affected, including the ventricle, atrium, or endothelium of large vessels. Predisposing factors for IE include pre-existing heart disease (eg, rheumatic valve disease), implantation of cardiac devices, intravenous drug use, and HIV infection [6], as well as skin diseases such as atopic dermatitis [7]. In patients with a predisposition to developing IE, a history of dental treatment should be considered in the diagnostic process, as such treatment increases the risk of bacteremia and subsequent disease [8]. The incidence of IE in HIV-infected patients who use intravenous drugs ranges from 6.3% to 34% regardless of the use of HAART (highly active antiretroviral therapy) [9]. Furthermore, IE in HIV-infected patients is more often localized on the right side of the heart [10]. This case study presents a patient with HIV and IE who experienced asystole during swallowing.

Case Report

A 35-year-old man with HIV infection was admitted to the Pulmonary Department for pneumonia and decompensation of type 1 diabetes mellitus in the presence of a systemic infection of unknown origin. Upon admission, the patient was in a moderate condition, lying down with contact disturbances, responding to pain stimuli, and only selectively and to a limited extent to verbal stimuli, exhibiting signs of sleepiness, sweating, and tachycardia (120 beats per minute) and tachypnea (35 breaths per minute). The blood pressure was 125/80 mmHg, and his oxygen saturation (SpO2) was 91%. The throat mucosa was observed to be dry with dried secretions. The skin exhibited numerous scars, lacerations, and small wounds. He was noted to be emaciated. Given the inability to conduct an interview with the patient, the patient’s history was obtained from his partner, which revealed a homosexual relationship, HIV and HCV (hepatitis C virus) infection, syphilis, secondary thrombocytopenia, diabetes, and penile condyloma. According to the history, the patient had a dental check-up several years previously, with no dental concerns at the time of admission and no cavities or caries. He was undergoing long-term antiviral treatment (bictegravir 50 mg, emtricitabine 200 mg, tenofovir 25 mg) and was concurrently taking antidepressants (fluoxetine 20 mg). Additionally, his partner reported inconsistent insulin administration, infrequent blood glucose monitoring, and long-term nicotine use. However, the partner denied the patient’s substance abuse. Prior to admission, the patient had been experiencing chest discomfort radiating to the left upper extremity and dyspnea for several days. Laboratory tests conducted upon admission revealed indeterminate glucose values. Subsequent measurement indicated a level of 736 mg/dL, along with a HbA1C of 13.3%. He had elevated inflammatory parameters, including C-reactive protein (CRP) at 430 mg/L and procalcitonin (PCT) at 6.85 ng/ml. Additionally, he had anemia, with a hemoglobin (HGB) level of 8.5 g/dl and red blood cell (RBC) count of 3.94×106/μl. Thrombocytopenia was also evident, with a platelet (PLT) count of 41×103/μl. Urinalysis revealed the presence of ketones and leukocytes. Significant hypernatremia was noted at admission (160 mmol/l). The concentration of potassium in the serum was 5.75 mmol/L, while the concentration of uric acid was 660 umol/L. The concentration of D-dimer was 20 μg/ml. Arterial blood gases revealed type 1 respiratory failure with compensated respiratory alkalosis (pH 7.41, pCO2 21.6 mmHg, pO2 59.3 mmHg, HCO3 13.4 mmol/L, BE −8.7 mmol/L, SpO2 91.7%), indicating the need for passive oxygen therapy (initially 2 L/min, with the flow rate subsequently increased as required). An intermediate axis electrocardiogram (ECG) revealed a sinus rhythm of 120 beats per minute, negative T-waves in aVL, V5–V6, and features of left ventricular hypertrophy. The initial chest X-ray demonstrated irregular macular thickening in all lung fields, predominantly in the peripheral regions (Figure 1).

During hospitalization, a multifaceted therapeutic regimen was initiated, encompassing steroid therapy, broad-spectrum antibiotic therapy (vancomycin and meropenem), antifungal treatment (fluconazole), and continuous insulin infusion modified based on glycemia measurements. Due to severe dehydration and difficulties with maintaining peripheral venous access significantly impairing proper IV fluid transfusion, a central line was placed by a consulting anesthesiologist. In view of the suspected diagnosis of pneumocystosis, sulfamethoxazole and trimethoprim were also included in the therapeutic regimen. In view of the anemia, 4 units of group-compatible red blood cell concentrate (CRC) were transfused.

Given the persistence of the presented disturbance of consciousness despite the normalization of glycemia and slight decrease of sodium concentration to 157 mmol/l, a computed tomography (CT) scan of the head with contrast was also conducted to exclude a potential head injury. The CT image of the brain did not reveal any discernible alterations. Despite a reduction in inflammatory markers and a return to normal blood glucose levels, there was no observable improvement in the patient’s condition. Moreover, he required higher a concentration of oxygen via nasal cannula. Consequently, further radiological investigations were conducted, including a CT angiogram of the lungs. This revealed the presence of multiple ground-glass lesions and indications of peripheral pulmonary embolism (PE) (Figure 2). However, due to thrombocytopenia, he was administered a reduced dose of low-molecular-weight heparin.

During hospitalization, a series of non-specific cardiac arrhythmias were observed, manifesting as several seconds of asystole (with the longest recorded asystole time of 4 seconds). These arrhythmic episodes were accompanied by transient episodes of chest tightness and coughing, particularly during swallowing (Figure 3, Video 1). As reported by his partner, the symptom had been present for several days prior to the patient’s admission, during which time it was erroneously identified as vomiting.

Despite consulting with neurologists, anesthesiologists, and internists on multiple occasions, the patient’s clinical picture remained unclear. Considering the occurrence of cardiac arrhythmias during structural heart defects such as valvular defects, we decided to consult a cardiologist. An ultrasound examination was conducted as part of the consultation, revealing a significant tricuspid valve vegetation measuring 31×13 mm (Figure 4, Video 2). Additionally, the left ventricular ejection fraction (LVEF) value was 40–45%, with a tricuspid valve gradient (TRV) of 35 mmHg. There were no peripheral vascular signs that could indicate IE, such as Osler’s nodules, Roth’s spots, or Janeway’s sign.

In the context of a diagnosis of IE, the patient was considered eligible for cardiac surgery. He was urgently transferred to the Cardiac Surgery Center for further evaluation and treatment. Upon admission to the cardiac surgery unit, he underwent a series of critical interventions. He was intubated and started on mechanical ventilation. Renal replacement therapy was initiated with continuous veno-venous hemodialysis, and circulatory support was provided using norepinephrine. During this time, blood culture results indicated the presence of Staphylococcus aureus. Consequently, targeted methicillin-sensitive Staphylococcus aureus (MSSA) therapy with cloxacillin and trimethoprim-sulfamethoxazole was initiated.

The patient underwent vegetation removal as the likely cause of severe tricuspid insufficiency and associated symptoms. Due to the high surgical risk and the patient’s critical condition, the vegetation was extracted using the AngioVac system during extracorporeal circulation. The procedure was performed under general anesthesia. The left groin was surgically prepared, exposing the femoral vein, and 2 purse-string sutures were placed. A venous cannula was inserted into the left femoral vein using the Seldinger technique. A 26F sheath was introduced into the right femoral vein, followed by the insertion of the AngioVac suction device. The AngioVac device was positioned under transesophageal echocardiography (TEE) and fluoroscopic guidance, successfully extracting the massive vegetation from the tricuspid valve (Figure 5). The TEE imaging of the vegetation extraction is shown in Video 3. Post-procedure TEE confirmed the absence of significant vegetations on the tricuspid valve; however, severe tricuspid regurgitation (TR) persisted, with a notable lack of tricuspid valve leaflets coaptation.

Given the thrombo-embolic risk, therapeutic anticoagulation with unfractionated heparin was administered. Due to a significant increase in inflammatory markers (an increase in the PCT level from 3.60 to 10.60 ng/ml), an empirical antibiotic therapy with meropenem was initiated. Given the presence of substantial edema and severe malnutrition, an intensive nutritional Angiola therapy was implemented via the gastrointestinal tract, including protein supplementation. Consistent dehydration management with torsemide was also initiated. Iron supplementation was started, but a transfusion of 7 units of packed red blood cells was required due to severe postoperative anemia (HGB 6.0 g/dl). After the procedure, he reported difficulties in maintaining steady breathing and substantial expectoration. However, he had a considerable reduction in chest pain in comparison with his pre-procedural condition. After removal of the vegetation from the tricuspid valve, he did not experience any further episodes of asystole.

The TR 2 weeks after the vegetation extraction procedure is demonstrated in Video 4.

Discussion

This case demonstrates a unique instance of a patient exhibiting asystole during swallowing, which was caused by IE. However, his initial therapy was focused on anti-inflammatory treatment along with normalization of diabetic and electrolytic decompensation during pneumonia. Nevertheless, despite the treatment, no discernible clinical improvement was observed. Continuous monitoring revealed non-specific cardiac arrhythmia during swallowing. The diagnosis of IE was established on the 2nd day of hospitalization after a detailed diagnosis and multidisciplinary consultation. Non-specific arrhythmias can present diagnostic difficulties due to the overlap of many conditions. The causes of asystole on swallowing can be due gastrointestinal, cardiovascular, neurological, and metabolic disorders. Similarly, our patient had multiple metabolic abnormalities such as hyperglycemia, hypernatremia, ketonuria, hyperkalemia, hyperuricemia that could affect the electrical function of the heart. Hypernatremia is associated with an elevated risk of mortality and an increased incidence of major cardiovascular diseases in men [11,12]. However, the arrhythmias observed in hypernatremia have been reported to be associated with prolongation of the QT interval, sinus tachycardia, a short PR interval, and diffuse ST depressions [13]. In our case, the arrhythmia during swallowing, as documented on the cardiac monitor with properly clipped electrodes, was subsequently confirmed by the physician through the absence of a palpable pulse. The transmission of infection to the surrounding myocardium causing IE can cause conduction disturbances, resulting in cardiac arrhythmias. The most common arrhythmias observed during IE are first-degree atrioventricular block, but more serious conditions such as complete heart block or bundle branch block can also manifest [14]. Changes in electrocardiography during IE are more common in homosexual men and in intravenous drug users [15]. However, ECG changes in IE are uncharacteristic or absent and can include atrioventricular and intraventricular blocks with variable frequency: atrioventricular block grade I (31%), left bundle branch anterior bundle branch block (22%), right bundle branch block (17%), left bundle branch block and atrioventricular block grade III (11%), and atrioventricular block grade II (8%); therefore, this test is not sufficient to assess for possible endocardial infection [16]; therefore, echocardiography should be performed in any patient with suspected IE. The cause of swallowing-induced syncope during IE in our case remains unexplored. It is worth considering the relationship between IE and vagus nerve stimulation and swallowing, as well as the presence of conduction system disorders in patients. In essence, swallowing rarely affects the heart rhythm and, when it does occur, it usually causes bradycardia, although cases of tachycardia have also been described [17]. As established previously, swallowing-related bradyarrhythmias are vagus nerve-dependent and may be associated with structural abnormalities of the heart or gastrointestinal tract [18]. Haumer et al [19] found an association between syncope-related swallowing and hypoxia; as they suggest, swallowing disorders can be the result of hypoxia, which intensifies the vagal reflex.

This issue is poorly understood, and future studies analyzing the above symptoms in more detail are needed. In addition to the observed cardiac arrhythmias, such patients can have high fever, features of cardiovascular and respiratory decompensation, cough, dizziness, syncope, or septic shock during IE [20]. Given the radiologic changes on the chest X-ray, it was incorrect to initially consider pneumonia as the underlying cause of our patient’s severe condition. He presented with features of respiratory failure that could have been explained by a diagnosis of pneumonia and PE with compatible clinical data, making it difficult to find the underlying cause of the condition. PE is one of the major causes of delayed diagnosis of IE [21]. It is also worth mentioning the increased incidence of PE events in right-sided IE. Hematologic changes, including leukocytosis, which was also observed in the present case, have been reported as one of the causes [22]. In our case, the PE appears to have been caused by vegetations on the tricuspid valve. Therefore, it is crucial in the therapeutic and diagnostic process to make an appropriate diagnosis to exclude IE in any patient with fever, PE, and active HIV infection. To date, asystolic dysphagia has not been described in patients with IE. A 2017 paper described a case of syncope while swallowing pills, with a 6.2-second interval of cardiac electrical activity in a 68-year-old woman with hypertension, bradycardia, dyslipidemia, and recently-diagnosed glomerulonephritis [20], the baseline ECG showed first-degree atrioventricular block, with no changes on echocardiography, and the gastroenterology examination revealed an esophageal hiatal hernia [23]. A British center reported a case of a 25-year-old woman with syncope on swallowing that had occurred over several years with solid food intake [24]. During hospitalization, she was found to have a 4.3-second pause in electrical activity of the heart, with symptoms worsening with dehydration. She had no other significant medical conditions, and no identifiable cause for this phenomenon was found. Similar to our patient, Chettri et al [25] described the case of a 71-year-old patient with 9-second asystole while drinking beverages (mainly carbonated) after fundoplication for severe gastroesophageal reflux disease. The patient had no other cardiovascular disease. In another case, a 39-year-old patient with diabetes mellitus and hypertension reported symptoms of chest tightness and dizziness related to swallowing during meals. An ECG revealed an asystole of 6.2 seconds while drinking cold beverages. The patient did not have any cardiovascular disease [26]. The incidence of infective endocarditis has remained similar over the years, at 3.3–7.0 cases per 100 000 patient-years (in the US population between 1950 and 2000), but the factors leading to the development of this disease are changing [27]. Of particular concern is the increasing role of intravenous drug use in IE. Nevertheless, iatrogenic predisposing factors for IE, such as intracardiac devices, central venous catheters, arteriovenous fistula for dialysis, and cardiac defects, still predominate [28]. In the intravenous drug user population, IE is more common in men, in HIV-positive patients, and in younger patients compared to non-IV-related IE [27]. HIV-positive patients with significant immunosuppression are expected to have a poorer prognosis [10], but with appropriate and regular HAART, ongoing viral infection does not significantly affect the course of IE [29]. The presence of bacterial vegetation on the right side of the heart in IV drug users is several times more common than on the left side, and in most cases it specifically affects the tricuspid valve [30]. There are several possible causes for this phenomenon. One theory involves the introduction of contaminants contained in an intravenous chemical that, depending on the direction of blood flow and penetration from the periphery to the right half of the heart, directly damages the endocardium [30]. The subsequent thrombus formation promotes vegetation deposition. The source of the pathogen may be the injection process itself. During the administration of the drug, there is a high risk of failure to maintain aseptic conditions and the introduction of the pathogen into the systemic circulation through a contaminated needle or the administration of bacteria present on the patient’s skin. The right heart therefore provides a specific filter for the right-sided circulation during intravenous access [30]. Another source of the pathogen may be an ongoing inflammatory process in another organ, including latent foci (eg, an untreated tooth, middle ear inflammation and abscess, and polymicrobial wound infection) [31]. In the present case, the patient’s skin was affected, indicating that it may have been the gateway to an IE infection. Additional confirmation appears to be MSSA infection, which is the most common bacterium causing purulent skin and soft-tissue infection [32]. Microbiologic diagnosis based on a positive blood culture is critical in identifying and assessing the susceptibility of the causative bacterium. IE is most often caused by Staphylococcus bacteria, followed by Streptococcus, Enterococcus, and gram-negative bacteria [20]. The notable rise in the prevalence of Staphylococcus aureus infections has been linked to an elevated risk of prolonged hospitalization and mortality [33]. A course of antibiotics is the usual treatment for IE, with the specific antibiotic selected based on the microorganism cultured from blood cultures, which can take 7 days. Therefore, it is imperative to initiate an empirical therapeutic regimen, typically a combination of vancomycin and gentamicin, which can treat the most common pathogens associated with IE [34]. Nevertheless, the rising prevalence of antibiotic resistance, particularly against Staphylococcus aureus, underscores the urgent need for development of novel antibiotics and combination therapy regimens [34]. The management of severe TR with large vegetations in critically ill patients presents significant challenges. In our case, intervention was deemed necessary due to the presence of severe TR unresponsive to diuretic therapy,and a large residual tricuspid vegetation measuring 31×13 mm, increasing the risk of embolic events (PE was present in this case) and hemodynamic instability. When evaluating treatment options, the risk-benefit ratio of each approach was carefully considered to determine the optimal course of action for this high-risk patient. The 2023 ESC guidelines recommend intervention for vegetations exceeding 20 mm in right-sided infective endocarditis (RSIE), especially when accompanied by significant right ventricular dysfunction, respiratory compromise, or increased embolic risk [20]. Open-heart surgery, the standard treatment for large vegetations and severe TR, offers the benefit of directly removing the vegetation and repairing or replacing the valve. However, the risks in our case were excessively high. The patient’s critical conditio – including dependence on mechanical ventilation, renal replacement therapy, and vasopressors (norepinephrine) – along with severe malnutrition and thrombocytopenia, significantly increased the likelihood of perioperative morbidity and mortality. Consequently, the potential benefits of surgery were outweighed by the substantial risks, making it an unsuitable option. Conservative management with antibiotics alone, while essential for controlling the infection, posed its own risks. Although non-invasive, this approach could not address the threat of the massive vegetation, leaving the patient vulnerable to further embolic events. Thus, in our opinion, the risk of ongoing complications without vegetation removal outweighed the benefit of avoiding procedural risks, rendering antibiotics alone insufficient. In contrast, the AngioVac system, a minimally invasive, catheter-based device for vegetation removal, offered a favorable risk-benefit profile. By enabling suction removal of the vegetation during extracorporeal circulation, it addressed the urgent need to reduce the infectious load and embolic risk without the extensive trauma of open surgery. While it does not correct the underlying valve dysfunction, the benefits of stabilizing the patient and averting immediate life-threatening complications outweighed the risks, and seemed to be a better option than surgery. This decision aligns with the 2023 ESC guidelines, which support less-invasive options like percutaneous aspiration for patients unfit for traditional surgery [20]. A review of the literature reveals that the AngioVac system has been successfully employed in similar cases. Zern et al [35] reported the successful use of the AngioVac system in a critically ill patient with right-sided infective endocarditis (RSIE), noting its efficacy in reducing the infectious load, decreasing the risk of further embolic events, and achieving clinical stability as a bridge to surgery [36]. A systematic review of 49 studies further corroborates this, emphasizing the high survival rate at discharge (93%) in patients undergoing AngioVac vegetectomy [37]. The most common risk factor identified was intravenous drug abuse and the primary indication for AngioVac usage was poor surgical candidacy (81%), similar to our case. In the present case, the AngioVac system was efficacious in debulking the vegetation, thereby improving clinical stability despite persistent severe TR. Post-procedure TEE confirmed the successful removal of the vegetation, although the severe TR persisted. This outcome is consistent with the findings of a systematic review that reported tricuspid regurgitation (TR) improvement in only 16% of cases and unchanged or worsened TR in 84% of cases [31]. These findings underscore the value of the AngioVac system as a viable alternative for managing RSIE in high-risk patients. The system offers a minimally invasive solution that can be lifesaving for patients who are unable to undergo traditional surgery. However, the limited improvement in TR and the lack of randomized controlled trials highlight the need for further research. Additionally, careful consideration and consensus by an endocarditis specialist team are crucial to balance the benefits and risks associated with this procedure. Following the AngioVac system’s successful removal of the tricuspid valve vegetation, patients with severe TR due to IE require a focused plan under cardiology oversight. Following the procedure, it is recommended to continue antibiotic therapy with cloxacillin for 6 weeks, based on Staphylococcus aureus sensitivity, with blood cultures and inflammatory markers monitored to ensure infection resolution. To manage acute TR-related fluid overload, patients should receive diuretic therapy, and inotropic support may still be required if hemodynamic instability persists after the intervention due to right ventricular dysfunction or ongoing TR. This should be supported by nutritional optimization and control of HIV and diabetes mellitus. For long-term management, patients should maintain diuretics to mitigate fluid retention, with beta-blockers considered if right-sided heart failure symptoms emerge, and afterload-reducing agents added if tolerated. Finally, patients should undergo transthoracic echocardiography every 3–6 months to assess TR severity and right ventricular function, guiding treatment adjustments. If heart failure symptoms persist or right ventricular dysfunction worsens, patients should be evaluated for tricuspid valve surgery after IE resolution and clinical stabilization. A meta-analysis by Yanagawa et al [38] comparing tricuspid valve repair versus replacement in IE suggests repair as the preferred approach, citing lower rates of recurrent IE (RR 0.17, P=0.004), reoperation (RR 0.26, P=0.04), and need for a pacemaker (RR 0.20, P<0.001), with no survival difference. Repair techniques preserve native anatomy and avoid life-long anticoagulation. However, in this case, extensive valve damage – potentially involving leaflet destruction or severe annular distortion – may necessitate replacement. If repair is unfeasible, replacement options include a bioprosthetic valve, avoiding anticoagulation but with limited durability, or a mechanical valve, offering longevity but requiring anticoagulation, complicated by the thrombocytopenia risk. The choice should reflect the patient’s age (35 years), bleeding profile, HIV status, and other factors considered by the multidisciplinary team.

Conclusions

Cardiac abnormalities during swallowing present a diagnostic difficulty, particularly in patients with multimorbidity. Most often, such disorders are associated with gastrointestinal dysfunction and cardiovascular or metabolic diseases. It is of the utmost importance to obtain a comprehensive medical history and perform a meticulous physical and imaging examination. In the absence of clear diagnostic methods, we cannot be certain that the arrhythmia in the case presented caused the chest pain and cough. Furthermore, there are no scientific reports to support these observations. Therefore, future studies using objective diagnostic methods are needed to verify the symptoms that may be present in a patient with IE. The case presented highlights that when there are indications of drug abuse, HIV infection, Staphylococcus aureus infection, PE, or fever, echocardiography may be an appropriate diagnostic procedure. In this case, this examination enabled the diagnosis of infective endocarditis. The patient was deemed a suitable candidate for surgical intervention due to the presence of a large vegetation and severe tricuspid regurgitation, which elevated the risk of embolic events and hemodynamic instability. Given the significant surgical risk, endovascular vegetation aspiration was performed as a minimally invasive alternative, with the dual objective of reducing the infectious load and stabilizing the patient. This case demonstrates the need for less invasive options in the treatment of high-risk patients when traditional surgery is not a viable option. A decision regarding further surgery for tricuspid regurgitation will be made after the successful treatment of infective endocarditis.