Citations

NISHIMURA, R.A. et al.: Hemodynamic and symptomatic consequences of ventricular pacing. After implantation of a ventricular demand pacemaker (VVI), occasional patients continue to have dizziness, syncope, or near syncope (“pacemaker syndrome”). To identify patients in whom VVI pacing may have deleterious effects, we compared cuff blood pressure responses to VVI pacing with blood pressure responses to atrioventricsler sequential pacing (DVI) or sinus rhythm in 50 consecutive patients. Patients with intact ventriculoatrial conduction had a much greater decrease in systolic blood pressure with VVI pacing (24 ± 11 mm Hg) than those with ventriculoatrial dissociation (−4 ± 15 mm Hg) (P<0.005). Patients who were in heart failure had a lesser decrease in blood pressure with VVI pacing than did those without failure (P<0.05); 13 of the 14 heart failure patients lacked ventriculoatrial conduction. Ten patients had symptomatic dizziness after VVI pacing; the incidence of symptoms was higher in patients with ventriculoatrial conduction (9 of 23) than in those without ventriculoatrial conduction (1 of 27) (P<0.003). We conclude that the presence of intact ventriculoatrial conduction appears to be a crucial determinent of the hemodynamic response to VVI pacing, and its presence may identify patients who are at risk for “pacemaker syndrome.”

A 33-year-old male with systemic lupus erythematosus (SLE) presented with acute abdominal pain and was found to have lupus mesenteric vasculitis on imaging and during exploratory laparotomy. Post laparotomy he continued to have persistent nausea and dyspepsia and an electrocardiogram showed evidence of an inferior ST elevation myocardial infarction (STEMI). Emergency cardiac catheterization showed evidence of thrombotic right coronary artery occlusion. His coronaries were otherwise normal with no evidence of underlying coronary artery disease. Extensive workup with trans-esophageal echo, serologies for antiphospholipid antibody syndrome (APS) and bubble study was negative. This effectively ruled out Libman–Sacks endocarditis, APS-induced arterial thrombus and paradoxical emboli as potential causes of his STEMI. By exclusion of other causes, the etiology of his STEMI was felt to be secondary to in-situ coronary artery thrombosis in the setting of active SLE. To the best of our knowledge, this is the first report of a patient with SLE presenting with both lupus mesenteric vasculitis and in-situ coronary arterial thrombosis in the absence of APS.

In this report, we describe the case of a 41‐year‐old man with hypertrophic cardiomyopathy presenting with right‐sided congestive heart failure symptoms. Noninvasive testing was suggestive, but non‐diagnostic for constrictive pericarditis (CP) and thus invasive hemodynamic catheterization was performed. The unique presence of both hypertrophic cardiomyopathy and constriction in this case led to lack of “modern” echocardiographic and invasive criteria for CP, based upon findings of enhanced ventricular dependence. However, classic hemodynamic criteria of early rapid filling with elevation and end‐equalization of diastolic pressures were present, and the patient ultimately received pericardiectomy with dramatic clinical improvement. © 2015 Wiley Periodicals, Inc.

Confirmation of the presence and magnitude of left ventricular outflow tract (LVOT) obstruction is a critical component of the evaluation of symptoms in patients with hypertrophic cardiomyopathy (HCM). The presence of LVOT obstruction in patients with severe symptoms refractory to pharmacologic therapy identifies a subgroup of HCM patients who may benefit from septal reduction therapy. Two‐dimensional echocardiography with continuous wave Doppler is the main tool for confirming the presence and severity of LVOT obstruction in HCM. However, when uncertainty remains following non‐invasive evaluation, invasive hemodynamics studies are required to confirm and quantify LVOT obstruction. In this manuscript we describe a series of 6 cases in which hemodynamic catheterization is instrumental in supplementing non‐invasive imaging in the assessment of LVOT obstruction in HCM. © 2015 Wiley Periodicals, Inc.

The management of women with mechanical heart valves during pregnancy remains difficult and controversial. There is no ideal anticoagulation regimen for this unique population, as there are inherent risks and benefits of each approach for both mother and fetus. There has been limited data available to guide the clinician in the optimal treatment strategy for an individual patient. The AHA/ACC Guidelines for the Management of Patients with Valvular Heart Disease created class recommendations for this population based upon current evidence, which is summarized in this review.

Background— Patients with severe tricuspid regurgitation (TR) frequently present with exertional fatigue and dyspnea, but the hemodynamic basis for exercise limitation in people with TR remains unclear. Methods and Results— Twelve subjects with normal left ventricular (LV) ejection fraction and grade ≥3 TR underwent high-fidelity invasive hemodynamic exercise testing with simultaneous expired gas analysis and were compared with 13 age- and sex-matched controls. At rest, TR subjects had lower pulmonary blood flow (3.6±0.4 versus 5.1±1.9 L/min; P =0.01), increased right atrial pressure (12±5 versus 4±1 mm Hg; P =0.0002), and higher pulmonary capillary wedge pressure (17±5 versus 9±3 mm Hg; P =0.0001). However, LV transmural pressure (pulmonary capillary wedge pressure−right atrial pressure), which reflects LV preload independent of right heart congestion and pericardial restraint, was similar in TR and controls (6±3 versus 4±2 mm Hg; P =0.3). With exercise, TR subjects displayed lower peak V O 2 (10.3±2.8 versus 13.8±4.2 mL/min per kg; P =0.02), lower pulmonary blood flow (6.4±1.3 versus 10.3±3.3 L/min; P =0.001), and less increase in pulmonary blood flow relative to V O 2 (+4.6±1.1vs +6.2±0.7; P =0.001). TR subjects displayed higher pulmonary capillary wedge pressure with exercise, but this was solely because of RA hypertension (27±9 versus 8±3 mm Hg; P <0.0001), because LV transmural pressure dropped with exercise in subjects with TR (−5±6 versus +3±3 mm Hg; P =0.0007), suggesting inadequate LV diastolic filling, despite high pulmonary capillary wedge pressure. Conclusions— Impaired exercise capacity in people with severe TR is related to low cardiac output reserve relative to metabolic needs, coupled with elevated systemic and pulmonary venous pressures. Left heart pressures are elevated with exercise in subjects with TR, despite low LV preload, secondary to enhanced ventricular interaction.

Background Atrial fibrillation ( AF ) is a common sequela of hypertrophic cardiomyopathy ( HCM ), but evidence on its prevalence, risk factors, and effect on mortality is sparse. We sought to evaluate the prevalence of AF , identify clinical and echocardiographic correlates, and assess its effect on mortality in a large high‐risk HCM population. Methods and Results We identified HCM patients who underwent evaluation at our institution from 1975 to 2012. AF was defined by known history (either chronic or paroxysmal), electrocardiogram, or Holter monitoring at index visit. We examined clinical and echocardiographic variables in association with AF . The effect of AF on overall and cause‐specific mortality was evaluated with multivariate Cox proportional hazards models. Of 3673 patients with HCM , 650 (18%) had AF. Patients with AF were older and more symptomatic ( P <0.001). AF was less common among patients with obstructive HCM phenotype and was associated with larger left atria, higher E/e’ ratios, and worse cardiopulmonary exercise tolerance (all P values<0.001). During median (interquartile range) follow‐up of 4.1 (0.2 to 10) years, 1069 (29%) patients died. Patients with AF had worse survival compared to those without AF ( P <0.001). In multivariate analysis adjusted for established risk factors of mortality in HCM , the hazard ratio (95% confidence interval) for the effect of AF on overall mortality was 1.48 (1.27 to 1.71). AF did not have an effect on sudden or nonsudden cardiac death. Conclusions In this large referral HCM population, approximately 1 in 5 patients had AF . AF was a strong predictor of mortality, even after adjustment for established risk factors.

Abstract To understand the biochemical events that occur in the airways after rhinovirus (RV) infection, we developed for the first time a model in which the cell lines from human mast cells (HMC-1) and basophils (KU812) can be infected with RV14, a major group RV. Viral infection was confirmed by demonstrating that viral titers in culture supernatants, and RV RNA increased with time. RV14 infection alone and a combination of PMA plus calcium ionophore A23187, did not increase histamine production by these cells, although IgE plus anti-IgE increased the histamine production. However, histamine content in the supernatants increased in response to PMA plus A23187, or IgE plus anti-IgE after RV14 infection. PMA plus A23187 or IgE plus anti-IgE induced the production of IL-8 and GM-CSF in supernatants of HMC-1 cells and IL-4 and IL-6 in supernatants of KU812 cells. RV14 infection further increased the production of the cytokines, whereas RV14 infection alone did not alter the production of the cytokines by these cells. An Ab to ICAM-1 inhibited RV14 infection of the cells and decreased the production of cytokines and histamine after RV14 infection. RV14 infection enhanced the increases in intracellular calcium concentration and activation of NF-κB by PMA plus A23187 in the cells. These findings suggest that RV14 infection may prime the cytokine and histamine production from mast cells and basophils and may cause airway inflammation in asthma.