Alejandro Perez-Verdia

Implantable cardioverter defibrillators and their role in heart failure progression

Patients with an implantable cardioverter defibrillator (ICD) implanted for primary prevention have an increased mortality rate if they receive appropriate and/or inappropriate ICD shocks. The most common cause of increased mortality is worsening heart failure. ICD shocks cause direct myocardial injury, contraction band necrosis, and fibrosis, and could induce persistent inflammation. These changes likely contribute to the ventricular dysfunction in patients who have a significantly depressed ejection fraction initially. One-third of the patients with ICDs have psychiatric disorders. Studies have demonstrated that the patients have decreased quality of life, including emotional dysfunction, during the month following an ICD shock. Patients with anxiety and depression have an activated hypothalamus-hypophysis-adrenal axis, increased sympathetic activity, and decreased vagal tone. Chronic sympathetic stimulation could directly affect the myocardium and worsen cardiac dysfunction. Consequently, although ICD implantation is life-saving, it may contribute to heart failure progression. Completed trials need reanalysis to determine whether there are unique characteristics of patients receiving shocks that might lead to additional therapy. Furthermore, the interaction between psychiatric disorders and ICD therapy needs more study.

Antibiotic‐induced Cardiac Arrhythmias

This review aims to clarify the underlying risk of arrhythmia associated with the use of macrolides and fluoroquinolones antibiotics. Torsades de pointes (TdP) is a rare potential side effect of fluoroquinolones and macrolide antibiotics. However, the widespread use of these antibiotics compounds the problem. These antibiotics prolong the phase 3 of the action potential and cause early after depolarization and dispersion of repolarization that precipitate TdP. The potency of these drugs, as potassium channel blockers, is very low, and differences between them are minimal. Underlying impaired cardiac repolarization is a prerequisite for arrhythmia induction. Impaired cardiac repolarization can be congenital in the young or acquired in adults. The most important risk factors are a prolonged baseline QTc interval or a combination with class III antiarrhythmic drugs. Modifiable risk factors, including hypokalemia, hypomagnesemia, drug interactions, and bradycardia, should be corrected. In the absence of a major risk factor, the incidence of TdP is very low. The use of these drugs in the appropriate settings of infection should not be altered because of the rare risk of TdP, except among cases with high-risk factors.

Prophylactic Implantation of Cardioverter Defibrillators in Idiopathic Nonischemic Cardiomyopathy for the Primary Prevention of Death: A Narrative Review

Implantable cardioverter defibrillator (ICD) therapy reduces sudden cardiac death rates and reduces mortality in patients with ischemic heart disease and low ejection fractions. One‐third of the deaths in patients with nonischemic cardiomyopathy are sudden. However, the efficacy of ICDs in the primary prevention of death in these patients is less clear. The most common cause of mortality in patients treated with ICDs is heart failure progression. ICD shocks can cause direct myocardial injury, fibrosis, inflammation, and adverse psychological outcomes, and these changes may contribute to the ventricular dysfunction in patients who already have a significantly depressed ejection fraction. We have reviewed the published randomized controlled trials and meta‐analysis of prophylactic ICD therapy in the primary prevention of death in patients with nonischemic cardiomyopathy. The individual randomized controlled trials do not report a statistically significant reduction of mortality unless the ICD treatment is added to cardiac resynchronization therapy, but the meta‐analysis did show a significant mortality reduction and favored ICD therapy in these patients. Medical management of many study participants was suboptimal, at least based on current guidelines. The patients with non‐ischemic cardiomyopathy have good outcomes with medical therapy, and ICD therapy in this relatively low‐risk population needs better selection criteria. Copyright

Effect of Pioglitazone on Platelet Aggregation in a Healthy Cohort

Background: Peroxisome proliferator-activated receptor (PPAR) agonists can favorably influence atheroma proliferation, lipoprotein metabolism and macrovascular complications. Pioglitazone, one of the thiazolidinedione compounds, is a PPAR ligand activator and a clinically important PPAR agonist. There is controversy in the literature about its potential antiplatelet effects. Its direct platelet inhibition is a novel hypothesis tested in animal models and in human populations with underlying diabetic and/or cardiovascular diseases. The present study was aimed to test the hypothesis of direct platelet aggregation inhibition with the use of pioglitazone in a healthy population. Methods: This prospective study was started after obtaining institutional review board approval. The platelet aggregation response to adenosine diphosphate, epinephrine, collagen and arachidonic acid was measured in healthy subjects before and after treatment with pioglitazone. The fasting lipid profile including total cholesterol, low-density lipoprotein, very-low-density lipoprotein and high-density lipoprotein was also measured. Results: Twenty subjects, 12 males and 8 females, were enrolled with a mean age of 31.5 ± 7.6 years (range 24–46). Two subjects did not complete the study and were excluded. The mean HbA1C was 5.4% (range 4.7–5.7). The study showed a non-significant platelet aggregation reduction after taking a 7-day pioglitazone course. The adenosine diphosphate-mediated platelet aggregation difference was not significant (p = 0.99); the arachidonic acid-mediated platelet aggregation difference was 0.6% (p = 0.93), for epinephrine 0.9% (p = 0.88) and for collagen 0.2% (p = 0.94). Further, it did not show a favorable response of lipoprotein profile with a non-significant reduction in all lipid panel values even though there is a slight reduction in total cholesterol, triglyceride, low-density lipoprotein and very low-density lipoprotein and a slight increase in high-density lipoprotein. Conclusions: We conclude that pioglitazone does not have a direct platelet aggregation inhibition effect in a healthy population, nor does it have a favorable effect on lipoprotein profile after a short treatment period.

Association of high-risk scores for obstructive sleep apnea with symptomatic bradyarrhythmias.

Background Obstructive sleep apnea (OSA) may have an association with bradyarrhythmias but often remains undiagnosed. Our aim was to determine if patients with a high risk of OSA attending our cardiology clinics had an association with symptomatic bradyarrhythmias, as this information might lead to changes in management strategy. Methods The Berlin questionnaire was used to assess risk of OSA in 190 patients, and they were divided into high-risk or low-risk groups. Demographic data and medical histories were recorded and patients groups were compared with t-tests and chi-square tests. A multivariate regression analysis was done to correct for confounding variables. Results The mean age of our sample population was 63.0 ± 14.7 years with a mean BMI of 29.5 ± 7.8 kg/m2. Using the Berlin questionnaire, 41.3% of the patients were classified as high risk; 15.7% of the patients had a known diagnosis of OSA. Between high-risk and low-risk groups, there was no significant difference in the prevalence of bradyarrhythmias (22.5 vs. 15.2% P = 0.21), symptomatic sinus node dysfunction (14.4 vs. 11.4% P = 0.66) or atrioventricular block (10.8 vs. 6.3% P = 0.33). A multivariable logistic regression analysis demonstrated that dyslipidemia had the strongest association with a high risk for OSA, but not bradyarrhythmias. Conclusions Based on the Berlin questionnaire, patients at a high risk for OSA did not have an increased prevalence of bradyarrhythmias. More studies are needed to assess the utility of evaluating patients with bradyarrhythmias for OSA prior to implanting permanent pacing devices.

Klippel-Trenaunay syndrome and radial artery coronary graft spasm.

A 75-year-old woman with known diagnosis of Klippel-Trenaunay syndrome presented with acute onset of chest pain, dyspnea and elevated cardiac enzymes. She had triple vessel coronary artery disease on subsequent coronary angiography. Given the unavailability of venous conduits secondary to lower extremity varicosities, coronary artery bypass grafting with radial and internal mammary arterial grafts was carried out. The radial artery graft went into spasm two days later and required intracoronary vasodilators to relieve the spasm. The patient remained hypotensive and finally expired.

Deep Sternal Wound Infection Caused by Group G Streptococcus after Open-Heart Surgery

We report the first case of deep sternal wound infection caused by group G Streptococcus after open-heart surgery. The patients clinical presentation was nonspecific and his diagnosis was delayed. Surgical debridement and a 4-week course of intravenous antibiotics consisting of sequential penicillin plus gentamicin/ceftriaxone led to recovery. Group G Streptococcus should be suspected as an important postoperative pathogen.

Risk factors and prevention of dabigatran-related gastrointestinal bleeding in patients with atrial fibrillation

Dabigatran, as compared with warfarin, was associated with lower rates of stroke and systemic embolism with similar rates of major hemorrhage. But it has a significantly higher risk of gastrointestinal bleeding (GIB). There are limited data on how to prevent GIB from dabigatran and what are the risk factors.

Effects of Alcohol and Illicit Substance Consumption in Patients with Infective Endocarditis

Alcohol and illicit drug use seem to compound every aspect of health, with cardiac and infectious complications as no exceptions. Not spared from the influence of alcohol and illicit drug use is the subject of infective endocarditis. This study assesses the prevalence of disease and risk of complications in patients with infective endocarditis who used alcohol, illicit drugs, or illicit drugs and alcohol. Medical records of the patients diagnosed with infective endocarditis were retrospectively reviewed. The study showed no causation between alcohol intake and prevalence of infective endocarditis but demonstrated significant decreased cardiac function, increased vegetation size, and incidence of embolic complications among drug and/or alcohol users compared to nondrug/alcohol users.

Atrial Fibrillation after Inhalational Lung Injury: A Troubling Complication of a Rare Problem

Atrial fibrillation (AF) has been associated with lung diseases like pneumonia and chronic obstructive pulmonary disease but has only infrequently been associated with inhalational lung injury. We report two cases of resistant AF, which developed in young healthy manual laborers shortly after inhalational lung injury due to massive quantity of pesticides and anhydrous ammonia, respectively. They had no evidence of valvular or structural heart disease and did not have any previous medical problems. The AF was resistant to antiarrhythmic drugs and required pulmonary vein isolation in first patient and possibly the second patient who is currently being evaluated for this procedure. These arrhythmias may reflect direct myocardial injury during and after exposure. Alternatively, multiple mechanisms can cause atrial fibrillation in lung diseases, including hypoxemia, acidemia, inflammatory mediators, and structural changes in the atria and ventricle, and these could lead to AF in inhalational lung injury cases. AF needs to be excluded when patients present with palpitations after inhalational lung injury, especially since, if unrecognized, AF may lead to complications, like thromboembolic phenomenon and tachycardiomyopathy.