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Effect of obstruction on longitudinal left ventricular shortening in hypertrophic cardiomyopathy

Barac, Ivan; Upadya, Shrikanth; Pilchik, Robert; Winson, Glenda; Passick, Michael; Chaudhry, Farooq A; Sherrid, Mark V
OBJECTIVES: We investigated the cause of the midsystolic drop (MSD) in left ventricular (LV) ejection velocities that are observed with hypertrophic cardiomyopathy (HCM) and severe obstruction. BACKGROUND: Dynamic obstruction is an important determinant of symptoms and adverse outcome. The MSD in velocity and flow occurs in patients with gradients >60 mm Hg. The nadir velocity in the LV occurs simultaneously with peak gradient. METHODS: We studied 36 patients with obstructive HCM and an MSD and compared them with 15 patients with HCM and no obstruction and with 25 age-matched normal control subjects. We measured LV ejection velocity proximal and distal to LV obstruction as well as tissue Doppler velocities and time intervals. RESULTS: The duration of contraction of both the septum and lateral wall is shorter in obstructed patients with the MSD than in nonobstructed HCM patients: septal contraction 203 +/- 68 ms vs. 271 +/- 41 ms (p < 0.001). Parallel reduction in the length of shortening was noted: 1.2 +/- 0.6 cm vs. 1.9 +/- 0.4 cm (p < 0.001). The ejection velocity nadir follows the septal and lateral peak velocities by 100 ms and 60 ms, respectively. The velocity nadir occurs as both walls rapidly decelerate to their premature termination: septal deceleration 79 +/- 35 cm/s2 vs. 48 +/- 21 cm/s2 (p < 0.001). With medical abolition of obstruction the MSD disappears and the duration and length of contraction normalizes. CONCLUSIONS: These data indicate that the MSD is caused by premature termination of LV segmental shortening and is a manifestation of systolic dysfunction.
PMID: 17367665
ISSN: 1558-3597
CID: 1571132

Angiographic findings and clinical correlates in patients with cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?

Wong SC; Sanborn T; Sleeper LA; Webb JG; Pilchik R; Hart D; Mejnartowicz S; Antonelli TA; Lange R; French JK; Bergman G; LeJemtel T; Hochman JS
OBJECTIVES: We sought to delineate the angiographic findings, clinical correlates and in-hospital outcomes in patients with cardiogenic shock (CS) complicating acute myocardial infarction. BACKGROUND: Patients with CS complicating acute myocardial infarction carry a grave prognosis. Detailed angiographic findings in a large, prospectively identified cohort of patients with CS are currently lacking. METHODS: We compared the clinical characteristics, angiographic findings, and in-hospital outcomes of 717 patients selected to undergo angiography and 442 not selected, overall and by shock etiology: left or right ventricular failure versus mechanical complications. RESULTS: Patients who underwent angiography had lower baseline risk and a better hemodynamic profile than those who did not. Overall, 15.5% of the patients had significant left main lesions on angiography, and 53.4% had three-vessel disease, with higher rates of both for those with ventricular failure, compared with patients who had mechanical complications. Among patients who underwent angiography, those with ventricular failure had significantly lower in-hospital mortality than patients with mechanical complications (45.2% vs. 57.0%; p = 0.021). Importantly, for patients with ventricular failure, in-hospital mortality also correlated with disease severity: 35.0% for no or single-vessel disease versus 50.8% for three-vessel disease. Furthermore, mortality was associated with the culprit lesion location (78.6% in left main lesion, 69.7% in saphenous vein graft lesions, 42.4% in circumflex lesions, 42.3% in left anterior descending lesions, and 37.4% in right coronary artery lesions), and Thrombolysis In Myocardial Infarction (TIMI) flow grade (46.5% in TIMI 0/1, 49.4% in TIMI 2 and 26% in TIMI 3). CONCLUSIONS: Patients who underwent angiographic study in the SHOCK Trial Registry had a more benign cardiac risk profile, more favorable hemodynamic findings and lower in-hospital mortality than those for whom angiograms were not obtained. Patients with CS caused by ventricular failure had more severe atherosclerosis, and a different distribution of culprit vessel involvement but lower in-hospital mortality, than those with mechanical complications. Overall in-hospital survival correlates with the extent of coronary artery obstructions, location of culprit lesion and baseline coronary TIMI flow grade
PMID: 10985708
ISSN: 0735-1097
CID: 38938

Postinfarction chest pain: Is pericarditis the cause? Maintain a high index of suspicion even after the patient is discharged

Hochman, J. S.; Pilchik, R. M.; Ratner, S. J.
Chest pain in a patient who has recently had an acute myocardial infarction (MI) may result from ischemia, pulmonary embolism, or pneumonia. Also consider pericarditis as a possible cause. Early postinfarction pericarditis occurs 2 to 4 days following acute MI, primarily in those with transmural infarction; it is usually heralded by low-grade fever and the development of a pericardial friction rub. Dressler's syndrome usually develops 1 to 28 weeks post-MI and is characterized by pleuropericarditis and constitutional symptoms (such as fever, malaise, myalgia, and arthralgia). Give aspirin as first-line therapy for early postinfarction pericarditis. Aspirin is also preferred for patients with Dressler's syndrome, although other NSAIDs (or brief corticosteroid therapy in complicated or refractory cases) may be used.
ISSN: 1040-0257
CID: 5477372

Post-MI Chest Pain: When to Suspect Pericarditis

[Pilchik, Robert; et al]
ISSN: 0194-259x
CID: 5477382