First use of a drug-eluting balloon in the treatment of acute renal artery occlusion and in-stent restenosis.

In-stent restenosis in a renal artery (RA) of a solitary functioning kidney is a serious complication of RA stenting. Drug-eluting balloons (DEB) have emerged as a novel way to manage restenosis. In this paper, the authors reported the first use of a DEB in the treatment of severe in-stent restenosis and thrombosis of a drug-eluting stent deployed in a RA. The patient presented with oligo-anuria and a serum creatinine (Scr) of 9 mg/dL that improved back to baseline of 2 mg/dL after the successful procedure. The optimal use of DEB in similar cases will have to be determined by larger clinical trials.

Plasma myeloperoxidase concentration predicts the presence and severity of coronary disease in patients with chest pain and negative troponin-T.

BACKGROUND: A non-negligible proportion of patients with chest pain with negative cardiac troponin may harbor a disrupted coronary plaque. A marker of plaque rupture upstream from myocardial necrosis may help identify high-risk patients among this patient population. The purpose of this study was to investigate the correlation of plasma myeloperoxidase (MPO) concentration and angiographic coronary disease among patients with suspected troponin-negative coronary syndromes. PATIENTS AND METHODS: Patients presenting with chest pain and negative cardiac troponin-T concentration and undergoing coronary angiography were enrolled in our study. Plasma MPO concentration was measured using a single blood sample collected prior to cardiac catheterization. The primary angiographic endpoint was the presence of at least one coronary stenosis causing a 70% or more diameter reduction; secondary endpoints were number of diseased vessels, presence of coronary thrombus, and lesion ulceration. The main clinical endpoint was coronary revascularization. RESULTS: Three hundred and eighty-nine patients were enrolled. Presence of coronary stenosis causing a 70% or more diameter reduction increased with increasing quartiles of myeloperoxidase concentration (P<0.0001), as did the presence of coronary thrombus (P<0.0001) and plaque ulceration (P<0.0001). The need for percutaneous coronary revascularization also increased with increasing quartiles of systemic myeloperoxidase levels (P<0.0001). Coronary surgical revascularization did not differ among myeloperoxidase quartiles. CONCLUSION: Among patients with chest pain without troponin elevation, a single measurement of plasma MPO concentration can help identify patients with a higher risk of having significant coronary stenoses and high-risk angiographic features.

Contrast-enhanced echocardiography for the diagnosis of apical hypertrophic cardiomyopathy.

The echocardiographic diagnosis of apical hypertrophic cardiomyopathy can be difficult in patients with poor acoustic windows. However, contrast-enhanced echocardiography can provide better images in these patients and lead to the correct diagnosis. We present a patient with apical hypertrophic cardiomyopathy who was diagnosed using contrast-enhanced echocardiography. The use of contrast-enhanced echocardiography for the diagnosis of apical hypertrophic cardiomyopathy in patients with poor acoustic windows is discussed and the experience in the literature reviewed.

Spontaneous coronary artery dissection: management options in the stent era.

Spontaneous coronary artery dissection (SCAD) is a rare cause of coronary obstruction, usually affecting women in the childbearing age. Pathogenetic mechanisms are elusive, and optimal treatment is not established. We describe a case of spontaneous coronary artery dissection that was successfully treated by coronary stenting. The published literature regarding the outcome of this modality of treatment in patients with SCAD is reviewed. A patient with spontaneous coronary artery dissection treated by stenting is described along with a review of the published literature regarding treatment of similar patients.

Cytokine imbalance in acute coronary syndrome.

The excessive mortality of coronary heart disease is attributed primarily to rupture and thrombotic transformation of the atherosclerotic plaque. Inflammation plays a critical role in plaque destabilization and vulnerability. Inflammation is not confined to the culprit segment but is convincingly widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic and hemodynamic factors are relevant to the pathological and clinical outcome. In addition to their fundamental role in thrombosis, there is ample evidence that platelets contribute significantly to promoting plaque inflammation. A new paradigm of unbalanced cytokine-mediated inflammation is emerging, providing diagnostic and therapeutic opportunity for intervention. Amplifying intrinsic anti-inflammatory mechanisms constitutes attractive avenues for future investigation.

Congestive heart failure: new paradigms and therapeutic targets.

Congestive heart failure is a major clinical and public health challenge. With increased aging, and advanced care of almost all other cardiac diseases, myocardial failure has become the single most common reason for hospitalization for patients older than 65. Conventional wisdom addressed heart failure as a hemodynamic perturbation consisting of congestion and limited cardiac output. Efforts intuitively focused on augmenting systolic function and clearing excessive pulmonary and systemic edema. Despite symptomatic improvement, mortality and functional deterioration continued unabated. Afterload reducing therapy emerged as an effective modality of improving cardiac function. Selective targeting of renin-angiotensin-aldosterone system (RAAS) was shown to be superior to alternative nonhormone-based approaches. These clinical observations gave impetus to the neurohumoral paradigm of heart failure. Whereas attention to the congestive aspects of heart failure remains an essential component of therapy, it is by no means sufficient to neutralize the complex and interactive pathogenic mechanisms which underlie this syndrome. Particularly relevant, is the asymptomatic stage of ventricular dysfunction which portend significant future structural and functional deterioration. Mounting evidence confirm the benefit of ACEI and ARB in attenuating ventricular remodeling and improving survival. This paper aims at reviewing the evidence which has led to the strongly held paradigm of neurohormonal basis of heart failure. Appropriate and evidence based therapeutic strategies are presented.