Accelerated Idioventricular Rhythm
Cardiac Complexes, Premature
Tachycardia
Arrhythmias, Cardiac
Electrocardiography
Chlorpheniramine
Heart Ventricles
Heart Block
Methylhistamines
Circadian Rhythm
Antitachycardia burst pacing for pleomorphic reentrant ventricular tachycardias associated with non-coronary artery diseases: a morphology specific programming for ventricular tachycardias. (1/8)
To study the role of antitachycardia burst pacing in patients with reentrant pleomorphic ventricular tachycardia (VT) associated with non-coronary artery diseases, the efficacy of antitachycardia pacing and appropriate antitachycardia pacing cycle length were evaluated in each pleomorphic VT morphology of seven patients. Seven patients were included in this study. Clinically documented pleomorphic VTs were reproduced in an electrophysiologic study. For each VT, rapid ventricular pacing was attempted from the apex of the right ventricle at a cycle length which was 20 ms shorter than that of VT and repeated after a decrement of the cycle length in steps of 10 ms until the VT was terminated or accelerated. All 16 VTs could be entrained by the rapid pacing, and 13 of the 16 VTs (81%) were terminated, whereas pacing-induced acceleration was observed in the other 3 VTs of the 3 patients. VT cycle length (VTCL), block cycle length (BCL) which was defined as the longest VT interrupting paced cycle length, %BCL/VTCL and entrainment zone which was defined as VTCL minus BCL, varied in each VT morphology of each patient. In two patients, antitachycardia pacing was effective in all VT morphologies and the maximum difference of the %BCL/VTCL among the pleomorphic VTs was less than 10%. Thus, antitachycardia pacing seemed to be beneficial for these patients. In the other 5 patients, a difference of more than 10% in %BCL/VTCL was observed among the pleomorphic VT morphologies and/or at least one VT morphology showed pacing-induced acceleration. Compared to the 13 terminated VTs, three accelerated VTs had a wide entrainment zone [160 +/- 44 vs 90 +/- 48 ms, p < 0.04] and small %BCL/VTCL [61 +/- 6 vs 77 +/- 11%,p<0.03]. In pleomorphic VTs associated with non-coronary artery diseases, responses to rapid pacing was not uniform; VT might be terminable or accelerated even in the same patient. We need to pay close attention when programming antitachycardia pacing in patients with pleomorphic VT. (+info)The D allele of the angiotensin-converting enzyme gene and reperfusion-induced ventricular arrhythmias in patients with acute myocardial infarction. (2/8)
The renin-angiotensin system may play a pivotal role in reperfusion ventricular arrhythmias (RVA). The purpose of this study was to investigate the association between angiotensin-converting enzyme (ACE) gene polymorphism and RVA in patients with acute myocardial infarction (AMI) in a case-control study. Patients who had undergone successful coronary intervention for AMI were enrolled (n= 127, male/female: 97/30, mean age, 62.6 years). The incidence of RVA was continuously monitored by ECG at a coronary care unit. The severity of ventricular arrhythmias was evaluated in terms of the Lown's grade and patients with a high risk of ventricular arrhythmias that may cause sudden cardiac death (Lown's grade > or =2) within 5 h of coronary intervention were defined as cases (n=59), and otherwise as controls (n=68). A receiver operating characteristic curve was used to determine the discriminatory ability of continuous variables and to produce dummy variables for use in a logistic regression analysis. Cases had a significantly higher body mass index, higher maximal levels of serum creatine kinase, and a shorter time preceding coronary intervention than controls. The severity of coronary atherosclerosis was similar between the 2 groups. The frequency distribution of ACE genotypes in cases differed from that in controls (II/ID/DD: 22.0%/52.6%/25.4% vs 44.1%/41.4%/14.7%, p<0.05, by the Mantel-Haenzel chi-square test). The ACE-D allele had additive and dominant effects with regard to the occurrence of significant ventricular arrhythmias after adjusting for other risk factors. The ACE-D allele may play a pivotal role in sudden cardiac death in patients with AMI. (+info)Five cases of aconite poisoning: toxicokinetics of aconitines. (3/8)
Aconite poisoning was examined in five patients (four males and one female) aged 49 to 78 years old. The electrocardiogram findings were as follows: ventricular tachycardia and ventricular fibrillation in case 1, premature ventricular contraction and accelerated idioventricular rhythm in case 2, AIVR in case 3, and nonsustained ventricular tachycardia in cases 4 and 5. The patient in case 1 was given percutaneous cardiopulmonary support because of unstable hemodynamics, whereas the other patients were treated with fluid replacement and antiarrhythmic agents. The main aconitine alkaloid in each patient had a half-life that ranged from 5.8 to 15.4 h over the five cases, and other detected alkaloids had half-lives similar to the half-life of the main alkaloid in each case. The half-life of the main alkaloid in case 1 was about twice as long as the half-lives in the other cases, and high values for the area under the blood concentration-time curve and the mean residence time were only observed in case 1. These results suggest that alkaloid toxicokinetics parameters may reflect the severity of toxic symptoms in aconite poisoning. (+info)Electrophysiological study and 'slow' ventricular tachycardia predict appropriate therapy: results from a single-centre implantable cardiac defibrillator follow-up. (4/8)
AIMS: To account for appropriate and inappropriate therapies and cardiac death (CD) in a cohort of consecutive implantable cardiac defibrillator (ICD) eligible patients and to identify baseline predictors of these outcomes. METHODS AND RESULTS: During follow-up of 288 consecutive ICD-treated patients, clinical, biochemical, echocardiographic, arteriographic, and electrophysiological (EP) data at baseline were individually matched with survival data and electrograms retrieved during device interrogation. Predictors of therapy and CD were identified by multivariate analyses. Eighty-eight per cent of cases were secondary prevention and 12% were primary prevention. About 770 patient-years of ICD follow-up were analysed. Median follow-up was 22.7 months. Forty-eight per cent of patients had appropriate therapy for at least one ventricular tachyarrhythmia. Seventy per cent of tachycardias were successfully treated with anti-tachy pacing alone. Overall risk of therapy was higher for patients with ischaemic heart disease (IHD) than with non-IHD (51 vs. 37%; P = 0.049). Low left ventricular ejection fraction (LVEF), positive EP study, and 'slow' ventricular tachycardia predicted appropriate therapy. Cardiac death was predicted by nephropathy, low LVEF, amiodarone use, and supraventricular tachycardia (SVT). Inappropriate therapy affected 12.2% of patients and was predicted by known SVT and IHD. CONCLUSION: Electrophysiological study and slow VT predicted appropriate therapy. Amiodarone use predicted CD. Inappropriate therapy remains an important issue largely predictable by SVT. (+info)Reentrant ventricular tachycardia originating in the right ventricular outflow tract: slow conduction identified by right coronary artery ostium pacing. (5/8)
A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was designated as the exit for the stable VT. Intriguingly, entrainment pacing from the ostium of the right coronary artery showed that the post-pacing interval was identical to VTCL. The stimulus to QRS interval was very long (340 ms) during entrainment with concealed fusion, and the right coronary artery ostium was therefore consistent with the VT reentry circuit inner loop or the upper portion of the VT reentry circuit exit. These findings suggest that the stable VT reentry circuit had a slow conduction zone from the ostium of the right coronary artery to the exit in the anterior septum RVOT. When radiofrequency catheter ablation was performed at the 2 exits of the anterior septum RVOT, both VTs then could not be induced. (+info)More pronounced diastolic left ventricular dysfunction in patients with accelerated idioventricular rhythm after reperfusion by primary percutaneous coronary intervention. (6/8)
OBJECTIVE: Reperfusion-induced accelerated idioventricular rhythm (AIVR) during primary percutaneous coronary intervention (pPCI) may be a sign of left ventricular (LV) dysfunction. We compared LV dynamic effects of reperfusion between patients with and without reperfusion-induced AIVR during pPCI for ST-elevation myocardial infarction (STEMI). METHODS: We studied 15 consecutive patients, who presented with their first acute anterior STEMI within 6 hours after onset of symptoms, and in whom LV pressure-volume (PV) loops were directly obtained during pPCI. Immediate effects of pPCI on LV function were compared between patients with (n = 5) and without (n = 10) occurrence of AIVR after reperfusion, as well as the direct effects of AIVR on LV function compared to sinus rhythm. RESULTS: Patients with reperfusion-induced AIVR showed more pronounced diastolic LV dysfunction before the onset of the arrhythmia, i.e., a delayed active relaxation expressed by Tau (53 +/- 15 vs. 39 +/- 6 ms; p = 0.03), a worse compliance curve (p = 0.01), and a higher end-diastolic stiffness (p = 0.07). At the end of the procedure, AIVR patients showed less improvement in diastolic LV function, indicated by a downward shift of the compliance curve (-3.1 +/- 2.3 vs. -7.5 +/- 1.4 mmHg; p = 0.001), a decrease in end-diastolic stiffness (13 +/- 18 vs. 34 +/- 15%; p = 0.03) and end-diastolic pressure (12 +/- 8 vs. 29 +/- 19%; p = 0.07). CONCLUSION: STEMI patients with reperfusion-induced AIVR after pPCI showed more pronounced diastolic LV dysfunction before and after AIVR than patients without AIVR, which suggests that diastolic LV dysfunction contributes to the occurrence of AIVR and that AIVR is a sign of diastolic LV dysfunction. (+info)Acute haemodynamic effects of accelerated idioventricular rhythm in primary percutaneous coronary intervention. (7/8)
(+info)Accelerated idioventricular rhythm associated with propranolol treatment in a child. (8/8)
Accelerated idioventricular rhythm (AIVR) is a ventricular arrhythmia most commonly seen in adults with underlying cardiac disease. It is important to establish the diagnosis when it occurs to differentiate this benign phenomenon from dangerous ventricular tachycardia. We present the case of a healthy child who developed episodes of AIVR associated with propranolol treatment. Her 24-hour electrocardiography recording showed AIVR with difference between sinus and ventricular beats. The arrhythmia resolved with the discontinuation of propranolol, and eventually the case was in sinus rhythm. This patient is the first case of AIVR associated with propranolol treatment in the literature. (+info)Accelerated idioventricular rhythm (AIVR) is a type of cardiac arrhythmia, which refers to an abnormal heart rhythm. In AIVR, the ventricles of the heart beat at a rate that is faster than normal but still slower than the rate seen in ventricular tachycardia. Specifically, the ventricular rate in AIVR is typically between 60 and 100 beats per minute.
AIVR originates from the ventricles of the heart, rather than from the normal pacemaker of the heart, which is located in the sinoatrial node in the right atrium. This means that the ventricles are activating themselves independently of the atria, resulting in a dissociation between the two chambers of the heart.
AIVR is often seen in patients who have underlying heart disease, such as myocardial infarction (heart attack), cardiomyopathy, or heart failure. It can also occur after cardiac surgery or other invasive procedures. In many cases, AIVR is benign and requires no treatment. However, if it is associated with hemodynamic instability or other symptoms, such as palpitations, shortness of breath, or chest pain, then further evaluation and treatment may be necessary.
Premature cardiac complexes, also known as premature heartbeats or premature ventricular contractions (PVCs), refer to extra or early heartbeats that originate in the lower chambers of the heart (the ventricles). These extra beats disrupt the normal rhythm and sequence of heartbeats, causing the heart to beat earlier than expected.
Premature cardiac complexes can occur in healthy individuals as well as those with heart disease. They are usually harmless and do not cause any symptoms, but in some cases, they may cause palpitations, skipped beats, or a fluttering sensation in the chest. In rare cases, frequent premature cardiac complexes can lead to more serious heart rhythm disorders or decreased heart function.
The diagnosis of premature cardiac complexes is usually made through an electrocardiogram (ECG) or Holter monitoring, which records the electrical activity of the heart over a period of time. Treatment is typically not necessary unless the premature complexes are frequent, symptomatic, or associated with underlying heart disease. In such cases, medications, cardioversion, or catheter ablation may be recommended.
Tachycardia is a medical term that refers to an abnormally rapid heart rate, often defined as a heart rate greater than 100 beats per minute in adults. It can occur in either the atria (upper chambers) or ventricles (lower chambers) of the heart. Different types of tachycardia include supraventricular tachycardia (SVT), atrial fibrillation, atrial flutter, and ventricular tachycardia.
Tachycardia can cause various symptoms such as palpitations, shortness of breath, dizziness, lightheadedness, chest discomfort, or syncope (fainting). In some cases, tachycardia may not cause any symptoms and may only be detected during a routine physical examination or medical test.
The underlying causes of tachycardia can vary widely, including heart disease, electrolyte imbalances, medications, illicit drug use, alcohol abuse, smoking, stress, anxiety, and other medical conditions. In some cases, the cause may be unknown. Treatment for tachycardia depends on the underlying cause, type, severity, and duration of the arrhythmia.
Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.
An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.
There are several types of cardiac arrhythmias, including:
1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.
Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.
Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.
Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.
During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.
ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.
Chlorpheniramine is an antihistamine medication that is used to relieve allergic symptoms caused by hay fever, hives, and other allergies. It works by blocking the action of histamine, a substance in the body that causes allergic symptoms. Chlorpheniramine is available in various forms, including tablets, capsules, syrup, and injection.
Common side effects of chlorpheniramine include drowsiness, dry mouth, blurred vision, and dizziness. It may also cause more serious side effects such as rapid heartbeat, difficulty breathing, and confusion, especially in elderly people or those with underlying medical conditions. Chlorpheniramine should be used with caution and under the supervision of a healthcare provider, particularly in children, pregnant women, and people with medical conditions such as glaucoma, enlarged prostate, and respiratory disorders.
It is important to follow the dosage instructions carefully when taking chlorpheniramine, as taking too much can lead to overdose and serious complications. If you experience any unusual symptoms or have concerns about your medication, it is best to consult with a healthcare provider.
The heart ventricles are the two lower chambers of the heart that receive blood from the atria and pump it to the lungs or the rest of the body. The right ventricle pumps deoxygenated blood to the lungs, while the left ventricle pumps oxygenated blood to the rest of the body. Both ventricles have thick, muscular walls to generate the pressure necessary to pump blood through the circulatory system.
Heart block is a cardiac condition characterized by the interruption of electrical impulse transmission from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This disruption can lead to abnormal heart rhythms, including bradycardia (a slower-than-normal heart rate), and in severe cases, can cause the heart to stop beating altogether. Heart block is typically caused by damage to the heart's electrical conduction system due to various factors such as aging, heart disease, or certain medications.
There are three types of heart block: first-degree, second-degree, and third-degree (also known as complete heart block). Each type has distinct electrocardiogram (ECG) findings and symptoms. Treatment for heart block depends on the severity of the condition and may include monitoring, medication, or implantation of a pacemaker to regulate the heart's electrical activity.
Methylhistamines are not a recognized medical term or a specific medical condition. However, the term "methylhistamine" may refer to the metabolic breakdown product of the antihistamine drug, diphenhydramine, which is also known as N-methyldiphenhydramine or dimenhydrinate.
Diphenhydramine is a first-generation antihistamine that works by blocking the action of histamine, a chemical released during an allergic reaction. When diphenhydramine is metabolized in the body, it is converted into several breakdown products, including methylhistamines.
Methylhistamines are not known to have any specific pharmacological activity or clinical significance. However, they can be used as a marker for the presence of diphenhydramine or its metabolism in the body.
Heart rate is the number of heartbeats per unit of time, often expressed as beats per minute (bpm). It can vary significantly depending on factors such as age, physical fitness, emotions, and overall health status. A resting heart rate between 60-100 bpm is generally considered normal for adults, but athletes and individuals with high levels of physical fitness may have a resting heart rate below 60 bpm due to their enhanced cardiovascular efficiency. Monitoring heart rate can provide valuable insights into an individual's health status, exercise intensity, and response to various treatments or interventions.
A circadian rhythm is a roughly 24-hour biological cycle that regulates various physiological and behavioral processes in living organisms. It is driven by the body's internal clock, which is primarily located in the suprachiasmatic nucleus (SCN) of the hypothalamus in the brain.
The circadian rhythm controls many aspects of human physiology, including sleep-wake cycles, hormone secretion, body temperature, and metabolism. It helps to synchronize these processes with the external environment, particularly the day-night cycle caused by the rotation of the Earth.
Disruptions to the circadian rhythm can have negative effects on health, leading to conditions such as insomnia, sleep disorders, depression, bipolar disorder, and even increased risk of chronic diseases like cancer, diabetes, and cardiovascular disease. Factors that can disrupt the circadian rhythm include shift work, jet lag, irregular sleep schedules, and exposure to artificial light at night.
Myocardial infarction (MI), also known as a heart attack, is a medical condition characterized by the death of a segment of heart muscle (myocardium) due to the interruption of its blood supply. This interruption is most commonly caused by the blockage of a coronary artery by a blood clot formed on the top of an atherosclerotic plaque, which is a buildup of cholesterol and other substances in the inner lining of the artery.
The lack of oxygen and nutrients supply to the heart muscle tissue results in damage or death of the cardiac cells, causing the affected area to become necrotic. The extent and severity of the MI depend on the size of the affected area, the duration of the occlusion, and the presence of collateral circulation.
Symptoms of a myocardial infarction may include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and sweating. Immediate medical attention is necessary to restore blood flow to the affected area and prevent further damage to the heart muscle. Treatment options for MI include medications, such as thrombolytics, antiplatelet agents, and pain relievers, as well as procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG).