Acute Cardiac Tamponade as a Complication of Pulmonary Vein Isolation Ablation.

Perioperative acute cardiac tamponade associated with perforation from pulmonary vein isolation (PVI) and radiofrequency catheter ablation (RFCA) for the treatment of refractory atrial fibrillation (AF) is rare. If not identified early and managed promptly, it can lead to decreased ejection fraction, hypotension, and ultimately death. We report a case of acute tamponade that was diagnosed and successfully managed following PVI and RFCA. A 49-year-old woman with a past medical history of paroxysmal AF and sick sinus syndrome presented to our hospital with intermittent episodes of palpitations and recurrent episodes of syncope. Given the drug-refractory AF, our patient underwent PVI and RFCA. A loop recorder was implanted for recurrent episodes of syncope, which revealed that she had sick sinus syndrome. During the current visit, transthoracic ECG revealed mild tricuspid regurgitation and trace pericardial effusion. Her left ventricle (LV) ejection fraction was 60%. A CT angiography of the pulmonary vessels and the aorta showed no evidence of pulmonary embolism, aortic aneurysm, or aortic dissection. However, there was an enlarged heart size and small bilateral pleural effusions. During a second PVI and RFCA, while in the operating room, the patient became hypotensive. A transesophageal echocardiogram (TEE) showed diastolic volume reduction in the right atrium and right ventricular and pericardial effusion. Intravenous (IV) resuscitation with lactated Ringer's solution and saline solution was rapidly given to the patient while performing percutaneous pericardiocentesis. In addition, packed red blood cells were transfused into the patient, and phenylephrine was given IV. There was 400 mL of blood drained from the pericardial sac, confirming the presence of acute cardiac tamponade. Following the pericardiocentesis, the patient became normotensive. A drainage tube was inserted into the pericardial space, which drained a total of 250 mL of sanguineous fluid over the next 48 hours after the procedure, after which it was removed without signs of persistent bleeding, and the patient was discharged. We conclude that her previous PVI and RFCA, and the anatomical distortion that might have resulted from her enlarged heart size, may have predisposed her to perforation and thus acute cardiac tamponade in this PVI and RFCA. Although perforation leading cardiac tamponade is rare during PVI and RFCA, the future focus when performing this procedure should be to (i) have a high index of suspicion for acute cardiac tamponade, (ii) use TEE and intracardiac echocardiography for early detection, and (iii) promptly manage the acute cardiac tamponade with pericardiocentesis, while giving IV fluid resuscitation and positive inotropes to hemodynamically stabilize the patient.

The pleiotropic effects of the hydroxy-methyl-glutaryl-CoA reductase inhibitors in renal disease.

It is well known that statins exert their main effect by inhibiting cholesterol synthesis through the inhibition of the 3-hydroxy-3-methyl-glutaryl-CoA reductase enzyme. The pleiotropic effects of statins, which are independent of their inhibition of cholesterol synthesis, have explained many of the beneficial effects of these drugs in a variety of disorders such as malignancies, infection, and sepsis, as well as in cardiovascular and rheumatologic disorders. However, the role of these drugs in renal disorders remains controversial. In the present review, we examine the most recent findings involving statins and renal disease among different clinical scenarios, including chronic kidney disease, contrast-induced nephropathy, renal injury after coronary artery bypass surgery, and renal transplant patients.

The use of nitrates in the prevention of contrast-induced nephropathy in patients hospitalized after undergoing percutaneous coronary intervention.

Contrast-induced nephropathy (CIN) is a significant cause of morbidity and mortality and effective strategies for its prevention are greatly needed. The purpose of this retrospective, single-center study was to investigate whether nitrate use during percutaneous coronary artery intervention reduces the incidence of CIN. Chart review of all individuals who underwent percutaneous coronary intervention (PCI) from April 2010 to March 2011 was done. Included in the study were patients who were admitted to the hospital after percutaneous coronary artery intervention and had baseline and follow-up creatinine measured. Patients with end-stage renal disease requiring dialysis and those patients with insufficient information to calculate Mehran score were excluded. There were 199 patients who met the eligibility criteria for inclusion in this study. In the identified population, postprocedure renal function was compared between 112 patients who received nitrates prior to coronary intervention and 87 who did not. Baseline characteristics were similar between the 2 groups. Contrast-induced nephropathy was defined as either a 25% or a 0.5 mg/dL, or greater, increase in serum creatinine during the first 48 to 72 hours after contrast exposure. Overall, 43 (21.6%) patients developed CIN post-PCI. Of the patients who received nitrates, 15.2% developed renal impairment when compared to 29.9% in those who did not (odds ratio [OR] = 0.42, 95% confidence interval [CI] 0.21-0.84, P = .014). Multivariate logistic regression analysis demonstrated that nitrate use was independently correlated with a reduction in the development of contrast nephropathy (OR = 0.334, 95% CI 0.157-0.709, P = .004). Additionally, of the various methods of nitrate administration, intravenous infusion was shown to be the most efficacious route in preventing renal impairment (OR = 0.42, 95% CI 0.20-0.90, P = .03). In conclusion, the use of nitrates prior to PCI, particularly intravenous nitroglycerin infusion, may be associated with a decreased incidence of CIN.

Renal denervation: current status and future applications.

Despite the variety of antihypertensive agents that are available, resistant hypertension remains a significant clinical problem and a substantial economic burden. Over the past several years, renal sympathetic denervation has been introduced as a potential therapeutic option for this clinical problem. It is a catheter-based procedure that is showing promising results and appears to be associated with minimal or low risk. Thus far, two completed clinical trials have demonstrated excellent safety and encouraging outcomes. A review of these trials is the focus of this article, in addition to the analysis of ongoing studies, and the possible future applications of this technique.

Comparison of 1.5 and 3 T BOLD MR to study oxygenation of kidney cortex and medulla in human renovascular disease.

OBJECTIVES: Imaging of the kidney using blood oxygen level dependent MR presents a major opportunity to examine differences in tissue oxygenation within the cortex and medulla applicable to human disease. We sought to define the differences between regions within kidneys and to optimize selection of regions of interest for study with 1.5 and 3 Tesla systems. MATERIALS AND METHODS: Studies in 38 subjects were performed under baseline conditions and after administration of furosemide intravenously to examine changes in R2* as a result of suppressing oxygen consumption related to medullary tubular solute transport. These studies were carried out in patients with atherosclerotic renal artery stenosis (n = 24 kidneys) or essential hypertension or nonstenotic kidneys (n = 39). All patients but one were treated with agents to block the renin angiotensin system (ACE inhibitors or angiotensin receptor blockers). For each kidney, 3 levels (upper pole, hilum, and lower pole) were examined, including 3 individual segments (anterior, lateral, and posterior). RESULTS: Low basal R2* levels in kidney cortex (12.06 +/- 0.84 s(-1)) at 1.5 Tesla reflected robust blood flow and oxygenation and agreed closely with values obtained at 3.0 Tesla (13.62 +/- 0.56 s(-1), NS). Coefficients of variation ranged between 15% and 20% between segments and levels at both field strengths. By contrast, inner medullary R2* levels were higher at 3 T (31.66 +/- 0.74 s(-1)) as compared with 1.5 T (22.19 +/- 1.52 s(-1), P < 0.01). Medullary R2* values fell after furosemide administration reflecting reduced deoxyhemoglobin levels associated with blocked energy-dependent transport. The fall in medullary R2* at 3.0 Tesla (-12.61 +/- 0.97 s(-1)) was greater than observed at 1.5 T (-6.07 +/- 1.38 s(-1), P < 0.05). Cortical R2* levels remained low after furosemide and did not vary with field strength. Correlations between measurements of defined cortical and medullary regions of interest within kidneys were greater at each sampling level and segment at 3.0 T as compared to 1.5 T. For patients studied with 3.0 T, furosemide administration induced a lesser fall in R2* in poststenotic kidneys at 3.0 T (-10.61 +/- 1.61 s(-1)) versus nonstenotic kidneys (-13.21 +/- 0.72 s(-1), P < 0.05). This difference was not evident in comparisons made at 1.5 T. The magnitude of furosemide-suppressible oxygen consumption at 3.0 T (-43%) corresponded more closely with reported experimental differences observed during direct measurement with tissue electrodes (45%-50%) than changes measured at 1.5 T. CONCLUSION: These results indicate that blood oxygen level dependent MR measurements at high field strength can better distinguish discrete cortical and inner medullary regions of the kidney and approximate measured differences in oxygen tension. Maneuvers that reduce oxygen consumption related to tubular solute transport allow functional evaluation of the interstitial compartment as a function of tissue oxygenation. Impaired response to alterations in oxygen consumption can be detected at 3 T more effectively than at 1.5 T and may provide real-time tools to examine developing parenchymal injury associated with impaired oxygenation.

Increased hypoxia and reduced renal tubular response to furosemide detected by BOLD magnetic resonance imaging in swine renovascular hypertension.

Oxygen consumption beyond the proximal tubule is mainly determined by active solute reabsorption, especially in the thick ascending limb of the Loop of Henle. Furosemide-induced suppression of oxygen consumption (FSOC) involves inhibition of sodium transport in this segment, which is normally accompanied by a marked decrease in the intrarenal deoxyhemoglobin detectable by blood oxygen level-dependent (BOLD)-magnetic resonance imaging (MRI). This study tested the hypothesis that the magnitude of BOLD-MRI signal change after furosemide is related to impaired renal function in renovascular hypertension. In 16 pigs with unilateral renal artery stenosis, renal hemodynamics, function, and tubular function (FSOC and fluid concentration capacity) were evaluated in both kidneys using MR and multidetector computerized tomography (MDCT) imaging. Animals with adequate FSOC (23.6 +/- 2.2%, P > 0.05 vs. baseline) exhibited a mean arterial pressure (MAP) of 113 +/- 7 mmHg, and relatively preserved glomerular filtration rate (GFR) of 60 +/- 4.5 ml/min, comparable to their contralateral kidney (66 +/- 4 ml/min, P > 0.05). In contrast, animals with low FSOC (3.1 +/- 2.1%, P = NS vs. baseline) had MAP of 124 +/- 9 mmHg and GFR (22 +/- 6 ml/min) significantly lower than the contralateral kidneys (66 +/- 4 ml/min, P < 0.05). The group with preserved GFR and FSOC showed an increase in intratubular fluid concentration as assessed by MDCT that was greater than that observed in the low GFR group, suggesting better preservation of tubular function in the former group. These results suggest that changes in BOLD-MRI after furosemide can differentiate between underperfused kidneys with preserved tubular function and those with tubular dysfunction. This approach may allow more detailed physiologic evaluation of poststenotic kidneys in renovascular hypertension than previously possible.

Regional decreases in renal oxygenation during graded acute renal arterial stenosis: a case for renal ischemia.

Ischemic nephropathy describes progressive renal failure, defined by significantly reduced glomerular filtration rate, and may be due to renal artery stenosis (RAS), a narrowing of the renal artery. It is unclear whether ischemia is present during RAS since a decrease in renal blood flow (RBF), O(2) delivery, and O(2) consumption occurs. The present study tests the hypothesis that despite proportional changes in whole kidney O(2) delivery and consumption, acute progressive RAS leads to decreases in regional renal tissue O(2). Unilateral acute RAS was induced in eight pigs with an extravascular cuff. RBF was measured with an ultrasound flow probe. Cortical and medullary tissue oxygen (P(t(O(2)))) of the stenotic kidney was measured continuously with sensors during baseline, three sequentially graded decreases in RBF, and recovery. O(2) consumption decreased proportionally to O(2) delivery during the graded stenosis (19 +/- 10.8, 48.2 +/- 9.1, 58.9 +/- 4.7 vs. 15.1 +/- 5, 35.4 +/- 3.5, 57 +/- 2.3%, respectively) while arterial venous O(2) differences were unchanged. Acute RAS produced a sharp reduction in O(2) efficiency for sodium reabsorption (P < 0.01). Cortical (P(t(O(2)))) decreases are exceeded by medullary decreases during stenosis (34.8 +/- 1.3%). Decreases in tissue oxygenation, more pronounced in the medulla than the cortex, occur despite proportional reductions in O(2) delivery and consumption. This demonstrates for the first time that hypoxia is present in the early stages of RAS and suggests a role for hypoxia in the pathophysiology of this disease. Furthermore, the notion that arteriovenous shunting and increased stoichiometric energy requirements are potential contributors toward ensuing hypoxia with graded and progressive acute RAS cannot be excluded.