Visualization of discrete microinfarction after percutaneous coronary intervention associated with mild creatine kinase-MB elevation.

BACKGROUND: Mild elevations in creatine kinase-MB (CK-MB) are common after successful percutaneous coronary interventions and are associated with future adverse cardiac events. The mechanism for CK-MB release remains unclear. A new contrast-enhanced MRI technique allows direct visualization of myonecrosis. METHODS AND RESULTS: Fourteen patients without prior infarction underwent cine and contrast-enhanced MRI after successful coronary stenting; 9 patients had procedure-related CK-MB elevation, and 5 did not (negative controls). The mean age of all patients was 61 years, 36% had diabetes, 43% had multivessel coronary artery disease, and all had a normal ejection fraction. Twelve patients (86%) received an intravenous glycoprotein IIb/IIIa inhibitor; none underwent atherectomy, and all had final TIMI 3 flow. Of the 9 patients with CK-MB elevation, 5 had a minor side branch occlusion during stenting, 2 had transient ECG changes, and none developed Q-waves. The median CK-MB was 21 ng/mL (range, 12 to 93 ng/mL), which is 2.3x the upper limit of normal. Contrast-enhanced MRI demonstrated discrete regions of hyperenhancement within the target vessel perfusion territory in all 9 patients. Only one developed a new wall motion abnormality. The median estimated mass of myonecrosis was 2.0 g (range, 0.7 to 12.2 g), or 1.5% of left ventricular mass (range, 0.4% to 6.0%). Hyperenhancement persisted in 5 of the 6 who underwent a repeat MRI at 3 to 12 months. No control patient had hyperenhancement. CONCLUSIONS: Contrast-enhanced MRI provides an anatomical correlate to biochemical evidence of procedure-related myocardial injury, despite the lack of ECG changes or wall motion abnormalities. Mild elevation of CK-MB after percutaneous coronary intervention is the result of discrete microinfarction.

Guiding catheter thrombectomy during percutaneous coronary interventions for acute coronary syndromes.

Despite the advancements in the pharmacological and mechanical treatment of acute coronary syndromes, intracoronary thrombus and distal embolization remain among the major limitations of percutaneous transluminal coronary interventions. We describe three cases in which intragraft or intracoronary thrombus was completely aspirated during PTCI using the guiding catheter. In the first case, a 4-cm-long unfragmented embolized thrombus was effectively and completely aspirated from a saphenous vein graft, with immediate restoration of normal flow. In the second case, multiple fragments of embolized thrombus were aspirated from a large right coronary artery, while in the third case, intragraft thrombus was electively aspirated. In each case, the index lesions were then successfully stented without complications. Cathet. Cardiovasc. Intervent. 49:192-196, 2000.

Echocardiographic predictors of an adverse response to a nifedipine trial in primary pulmonary hypertension: diminished left ventricular size and leftward ventricular septal bowing.

BACKGROUND: The clinical course in primary pulmonary hypertension (PPH) is improved by calcium channel blocker therapy in those with a favorable hemodynamic response during a trial of high-dose oral nifedipine. Although trials of nifedipine are performed only in patients who demonstrate pulmonary vasodilator reserve to short-acting agents, this response does not predict the safety of nifedipine treatment, which can result in severe first-dose hypotension and death. STUDY OBJECTIVES: To identify echocardiographic parameters that predict first-dose nifedipine-induced hypotension in patients with PPH. METHODS: The pretrial echocardiograms of 23 consecutive PPH patients (mean age, 42.3 +/- 13 years; 77% female) undergoing evaluation of pulmonary vasodilator reserve with nifedipine were analyzed. Patients were classified as those who suffered first-dose nifedipine hypotension (group 1) and those who did not (group 2). Echocardiographic measures of chamber size and septal geometry in the two groups were compared. RESULTS: Five measures reflecting diminished left ventricular (LV) size and leftward ventricular septal bowing were found to be associated with nifedipine hypotension: LV transverse diameter in systole (LVDs; p = 0.007), LV transverse diameter in diastole (LVDd; p = 0.05), LV area in systole (LVAs; p = 0.009), LV area in diastole (LVAd; p = 0.03), the ratio of RV to LVAs (p = 0. 02), and leftward ventricular septal bowing (p = 0.01). The LV dimensions found to best predict nifedipine-induced hypotension were LVDs < 2.7 cm, LVDd < 4.0 cm, LVAs < 15.5 cm(2), and LVAd < 20.0 cm(2). CONCLUSIONS: Readily available echocardiographic parameters in patients with PPH are predictive of nifedipine-induced hypotension, and can be used to select patients in whom a trial of nifedipine should be avoided.

Emergency extracorporeal membrane oxygenation (ECMO)-supported percutaneous coronary interventions in the fibrillating heart.

We describe two cases of refractory ventricular fibrillation complicating transcatheter interventional procedures. Extracorporeal membrane oxygenation was used in each to support percutaneous coronary revascularization in the fibrillating heart as a means of facilitating successful restoration of sinus rhythm. Cathet. Cardiovasc. Intervent. 48:402-405, 1999.

How to manage primary pulmonary hypertension. Giving hope to patients with a life-threatening illness.

Primary pulmonary hypertension presents a challenge to practicing physicians, in both diagnosis and management. Exposure to anorexigens and complaints of dyspnea and fatigue should prompt careful physical examination and Doppler echocardiography to assess patients for pulmonary hypertension. The burden on office practitioners is heavy, considering how often fatigue and dyspnea are reported, but the key is recognizing when these findings are out of proportion to the patient's well appearance. The discovery of epoprostenol therapy has revolutionized the approach to primary pulmonary hypertension. It has markedly improved quality of life and extended survival in patients with the condition, and it has changed the physician's role from providing emotional support to dying patients to providing management of a chronic disease.

How to manage secondary pulmonary hypertension.

Establishing an underlying cause and treatment plan for patients with pulmonary hypertension presents a significant challenge to practicing physicians. Doppler echocardiography is a simple, cost-effective tool for detecting pulmonary hypertension and evaluating right ventricular function. Nonspecific therapy (use of digoxin and diuretics, anticoagulation) for pulmonary hypertension and right ventricular failure achieves a degree of symptomatic improvement and should be considered in patients with moderate to severe disease. CTEPH should be considered in patients with dyspnea. Because severs forms of pulmonary hypertension usually are not discovered until late in the disease course, a high level of suspicion is required when evaluating symptoms and risk factors consistent with pulmonary vascular disease. Pulmonary hypertension is classified as idiopathic, or primary, when no secondary cause can be identified. Primary pulmonary hypertension is a devastating disease that largely affects young women. Significant advances in treatment have been made and will be discussed in detail in part 2 of this article.

Inhaled nitric oxide in primary pulmonary hypertension: a safe and effective agent for predicting response to nifedipine.

OBJECTIVES: The purpose of this study was to assess the utility of inhaled nitric oxide (NO), a selective pulmonary vasodilator, for predicting the safety and acute hemodynamic response to high-dose oral nifedipine in primary pulmonary hypertension (PPH). BACKGROUND: A significant decrease in pulmonary vascular resistance with an oral nifedipine challenge is predictive of an improved prognosis, and potential clinical efficacy in PPH. However, the required nifedipine trial carries significant first-dose risk of hypotension. While inhaled NO has been recommended for assessing pulmonary vasodilator reserve in PPH, it is not known whether it predicts the response to nifedipine. METHODS: Seventeen patients with PPH undergoing a nifedipine trial were assessed for hemodynamic response to inhaled NO at 80 parts per million for 5 minutes. The nifedipine trial consisted of 20 mg of nifedipine hourly for 8 hours unless limited by hypotension or intolerable side effects. Patients were classified as responders and nonresponders with positive response defined as > or =20% reduction in mean pulmonary artery pressure (mPA) or pulmonary vascular resistance (PVR) with the vasodilator administration. RESULTS: NO was safely administered to all participants. Seven of 17 (41.2%) responded to NO, and 8 of the 17 to nifedipine (47.1%). Nifedipine was safely administered in 14 of the 17. Three suffered either mild or severe hypotension, including one death. All NO responders also responded to nifedipine, and 9 of the 10 NO nonresponders were nifedipine nonresponders, representing a sensitivity of 87.5%, specificity of 100%, and overall predictive accuracy of 94%. All NO responders tolerated a full nifedipine trial without hypotension. There was a highly significant correlation between the effects of NO and nifedipine on PVR (r=0.67, p=0.003). CONCLUSIONS: The pulmonary vascular response to inhaled NO accurately predicts the acute hemodynamic response to nifedipine in PPH, and a positive response to NO is associated with a safe nifedipine trial. In patients comparable with those evaluated, a trial of nifedipine in NO nonresponders appears unwarranted and potentially dangerous.