Atherosclerosis is chronic disease, the prevalence of which has increased steadily as the population ages. Vascular injury is believed to be critical initiating event in pathogenesis of spontaneous atherosclerosis. Syndrome of accelerated atherosclerosis has been classically described in patients undergoing heart transplantation, coronary artery bypass graft, and percutaneous transluminal coronary angioplasty. In contrast to spontaneous atherosclerosis, denuding endothelial injury followed by thrombus formation and initial predominant smooth muscle cell proliferation is believed to be playing a significant role in accelerated atherosclerosis. There is no universal definition of rapid progression of atherosclerosis. However most studies describing the phenomenon have used the following definition: (i) > or = 10% diameter reduction of at least one preexisting stenosis > or = 50%, (ii) > or = 30% diameter reduction of a preexisting stenosis <50%, and (iii) progression of a lesion to total occlusion within few months. Recent studies have described the role of coronary vasospasm, human immunodeficiency virus, various inflammatory markers, and some genetic mutations as predictors of rapid progression of atherosclerosis. As research in the field of vascular biology continues, more factors are likely to be implicated in the pathogenesis of rapid progression of atherosclerosis.
The risk factor profile and the angiographic involvement differ considerably in the high-risk younger adults and substantiate the need for an aggressive approach directed toward primary and secondary preventions of premature cardiovascular disease.
A ortic dissection is a rare and potentially fatal sequela of percutaneous coronary intervention (PCI). The exact prevalence of aortic dissection after PCI is unknown, because occurrences might be unreported. The first case was reported in 1992. 1 We found 86 published instances 1-62 and have categorized these in detail. In addition, we present 2 new cases of aortic dissection consequent to PCI, and we discuss their specific treatment. Case Reports Patient 1A 52-year-old hypertensive man presented with acute inferior ST-segment-elevation MI (STEMI). He had a distant history of inferior myocardial infarction (MI) that had been treated with placement of a drug-eluting stent. At the current presentation, he was immediately taken for cardiac catheterization. Initial views of the left coronary system with use of a 6F Judkins left (JL)4 diagnostic catheter revealed no significant lesions. Views of the right coronary artery (RCA), examined with use of a 6F Judkins right (JR)4 diagnostic catheter, showed occlusion of the original proximal RCA stent. The diagnostic catheter was immediately removed, and a 6F JR4 guide catheter was used without difficulty to engage the RCA. A 180-cm Asahi Prowater Flex guidewire (Abbott Vascular, part of Abbott Laboratories; Abbott Park, Ill) was inserted into the RCA but could not cross the culprit lesion. This wire was exchanged for a 190-cm Hi-Torque Whisper guidewire (Abbott Vascular), and the lesion was successfully crossed with support from a 1.5 × 15-mm Maverick Over-the-Wire Balloon Catheter (Boston Scientific Corporation; Natick, Mass). Two brief inflations were done at pressures of 12 atm within the stent for 10 s each. The wire was upgraded to a 300-cm Asahi Prowater Flex wire while the Maverick balloon was still inside the artery. The patient reported chest pain, and his systolic blood pressure (SBP) fell to 78 mmHg. The balloon was removed. An angiogram showed dissection of the proximal RCA, extending retrograde into the right aortic cusp and ascending aorta (Fig. 1). In addition, slow flow and evidence of thrombus were noted in the RCA. A Pronto V3 extraction catheter (UDG Healthcare plc; Dublin, Ireland) was immediately inserted, and manual-aspiration thrombectomy was performed. Then, a 3.5 × 28-mm Vision ® bare-metal stent (Abbott Vascular), deployed in the proximal RCA at a pressure of 12 atm, was extended into the ostium to seal the dissection flap (Fig. 2).
Case ReportIn January 2013, a 41-year-old man, a heavy smoker who had little medical or surgical history, presented with New York Heart Association functional class III-IV dyspnea, which had worsened progressively over the preceding week and had been associated with subjective fevers, chills, and infrequent episodes of chest pain. On physical examination, the patient had a blood pressure of 96/45 mmHg, a pulse rate of 124 beats/ min, a respiratory rate of 24 breaths/min, and a temperature of 102.5 °F. Cardiac examination revealed the point of maximum impulse to be in the left 5th intercostal space at the mid-clavicular line; auscultation revealed an S 3 gallop at the mitral area, with a grade 4/6 holosystolic murmur best heard over the apex. The electrocardiogram showed sinus tachycardia without evidence of ischemic ST-T changes. The chest radiograph showed a normal cardiac silhouette with signs of pulmonary venous congestion.A 2-dimensional (2D) transthoracic echocardiogram (TTE) showed a membranelike structure extending from the superior LA wall to the base of the posterior mitral leaflet, creating a false lumen that partly occluded the true LA chamber-a picture consistent with LA free-wall dissection. Attached to the lower end of this membrane was a large mass with multiple finger-like projections (Fig. 1). Color-flow Doppler mode revealed a central jet of moderate mitral regurgitation caused by lack of coaptation of the mitral valve leaflets. Additional moderate-to-severe systolic flow was detected-this from the left ventricle into the false lumen, through a perforated posterior mitral leaflet (Fig. 2). Mild pericardial effusion was also noted. These findings were confirmed by a transesophageal echocardiogram (TEE) (Fig. 3). The dissection membrane caused no pulmonary vein obstruction.On the basis of the patient's clinical presentation, we obtained blood cultures and began broad-spectrum antibiotic therapy; however, within one hour of his presentation (and before surgical intervention), the patient died of cardiogenic shock refractory to medical treatment. Three blood cultures grew methicillin-sensitive Staphylococcus aureus.Although no definitive pathologic diagnosis by autopsy was available, the positive blood cultures, together with the 2D TTE and TEE findings in a patient with such a clinical presentation, are highly consistent with the diagnosis of infective endocarditis of the mitral valve. The formation of a large mitral valve vegetation appears to have
Quadricuspid aortic valve (QAV) is a rare congenital cardiac anomaly causing aortic regurgitation usually in the fifth to sixth decade of life. Earlier, the diagnosis was mostly during postmortem or intraoperative, but now with the advent of better imaging techniques such as transthoracic echocardiography, transesophageal echocardiography (TEE), and cardiac magnetic resonance imaging, more cases are being diagnosed in asymptomatic patients. We present a case of a 39-year-old male who was found to have QAV, with the help of TEE, while undergoing evaluation for a diastolic murmur. The patient was found to have Type B QAV with moderate aortic regurgitation. We also present a brief review of classification, pathophysiology, and embryological basis of this rare congenital anomaly. The importance of diagnosing QAV lies in the fact that majority of these patients will require surgery for aortic regurgitation and close follow-up so that aortic valve replacement/repair is done before the left ventricular decompensation occurs.
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